Shear-induced endothelial mechanotransduction: The interplay between reactive oxygen species (ROS) and nitric oxide (NO) and the pathophysiological implications

Hsyue-Jen Hsieh, Ching-Ann Liu, Bin Huang, Anne-Hh Tseng, Danny-Ling Wang

Research output: Contribution to journalArticle

121 Citations (Scopus)

Abstract

Hemodynamic shear stress, the blood flow-generated frictional force acting on the vascular endothelial cells, is essential for endothelial homeostasis under normal physiological conditions. Mechanosensors on endothelial cells detect shear stress and transduce it into biochemical signals to trigger vascular adaptive responses. Among the various shear-induced signaling molecules, reactive oxygen species (ROS) and nitric oxide (NO) have been implicated in vascular homeostasis and diseases. In this review, we explore the molecular, cellular, and vascular processes arising from shear-induced signaling (mechanotransduction) with emphasis on the roles of ROS and NO, and also discuss the mechanisms that may lead to excessive vascular remodeling and thus drive pathobiologic processes responsible for atherosclerosis. Current evidence suggests that NADPH oxidase is one of main cellular sources of ROS generation in endothelial cells under flow condition. Flow patterns and magnitude of shear determine the amount of ROS produced by endothelial cells, usually an irregular flow pattern (disturbed or oscillatory) producing higher levels of ROS than a regular flow pattern (steady or pulsatile). ROS production is closely linked to NO generation and elevated levels of ROS lead to low NO bioavailability, as is often observed in endothelial cells exposed to irregular flow. The low NO bioavailability is partly caused by the reaction of ROS with NO to form peroxynitrite, a key molecule which may initiate many pro-atherogenic events. This differential production of ROS and RNS (reactive nitrogen species) under various flow patterns and conditions modulates endothelial gene expression and thus results in differential vascular responses. Moreover, ROS/RNS are able to promote specific post-translational modifications in regulatory proteins (including S-glutathionylation, S-nitrosylation and tyrosine nitration), which constitute chemical signals that are relevant in cardiovascular pathophysiology. Overall, the dynamic interplay between local hemodynamic milieu and the resulting oxidative and S-nitrosative modification of regulatory proteins is important for ensuing vascular homeostasis. Based on available evidence, it is proposed that a regular flow pattern produces lower levels of ROS and higher NO bioavailability, creating an anti-atherogenic environment. On the other hand, an irregular flow pattern results in higher levels of ROS and yet lower NO bioavailability, thus triggering pro-atherogenic effects. © 2014 Hsieh et al.; licensee BioMed Central Ltd.
Original languageEnglish
JournalJournal of Biomedical Science
Volume21
Issue number1
DOIs
Publication statusPublished - 2014
Externally publishedYes

Fingerprint

Reactive Oxygen Species
Nitric Oxide
Flow patterns
Endothelial cells
Endothelial Cells
Biological Availability
Blood Vessels
Reactive Nitrogen Species
Homeostasis
Hemodynamics
Shear stress
Nitration
Molecules
Peroxynitrous Acid
NADPH Oxidase
Protein S
Post Translational Protein Processing
Vascular Diseases
Gene expression
Tyrosine

Keywords

  • Endothelial cell
  • Flow pattern
  • Mechanotransduction
  • Nitric oxide (NO)
  • Reactive oxygen species (ROS)
  • Shear stress
  • calcium calmodulin dependent protein kinase II
  • calmodulin
  • endothelial leukocyte adhesion molecule 1
  • endothelial nitric oxide synthase
  • heme oxygenase 1
  • hydroxymethylglutaryl coenzyme A reductase kinase
  • immunoglobulin enhancer binding protein
  • intercellular adhesion molecule 1
  • kruppel like factor 2
  • messenger RNA
  • monocyte chemotactic protein 1
  • nitric oxide
  • oxidized low density lipoprotein
  • peroxynitrite
  • reactive nitrogen species
  • reactive oxygen metabolite
  • reduced nicotinamide adenine dinucleotide phosphate oxidase
  • regulator protein
  • superoxide
  • thioredoxin 1
  • thioredoxin reductase 1
  • transcription factor AP 1
  • transcription factor Nrf2
  • tyrosine
  • unclassified drug
  • uncoupled endothelial nitric oxide synthase
  • vascular cell adhesion molecule 1
  • xanthine oxidase
  • antioxidant responsive element
  • atherogenesis
  • blood vessel reactivity
  • cardiovascular disease
  • disease association
  • endothelial dysfunction
  • endothelium cell
  • enzyme activation
  • enzyme activity
  • enzyme phosphorylation
  • flow kinetics
  • gene expression regulation
  • hemodynamics
  • homeostasis
  • laminar flow
  • mechanotransduction
  • mitochondrial membrane potential
  • mitochondrial respiration
  • nitration
  • nitrosylation
  • oscillation
  • oxidation reduction reaction
  • oxidative phosphorylation
  • pathophysiology
  • priority journal
  • protein binding
  • protein expression
  • protein modification
  • protein processing
  • proton transport
  • pulsatile flow
  • review
  • s glutathionylation
  • s nitrosylation
  • shear stress
  • tyrosine nitration
  • vascular endothelium
  • genetics
  • human
  • mechanical stress
  • metabolism
  • oxidative stress
  • signal transduction
  • Hemodynamics
  • Humans
  • Mechanotransduction, Cellular
  • Nitric Oxide
  • Oxidative Stress
  • Protein Processing, Post-Translational
  • Reactive Nitrogen Species
  • Reactive Oxygen Species
  • Signal Transduction
  • Stress, Mechanical

Cite this

Shear-induced endothelial mechanotransduction: The interplay between reactive oxygen species (ROS) and nitric oxide (NO) and the pathophysiological implications. / Hsieh, Hsyue-Jen; Liu, Ching-Ann; Huang, Bin; Tseng, Anne-Hh; Wang, Danny-Ling.

In: Journal of Biomedical Science, Vol. 21, No. 1, 2014.

Research output: Contribution to journalArticle

@article{b22586eada1c40608e9c5d3941fb33c9,
title = "Shear-induced endothelial mechanotransduction: The interplay between reactive oxygen species (ROS) and nitric oxide (NO) and the pathophysiological implications",
abstract = "Hemodynamic shear stress, the blood flow-generated frictional force acting on the vascular endothelial cells, is essential for endothelial homeostasis under normal physiological conditions. Mechanosensors on endothelial cells detect shear stress and transduce it into biochemical signals to trigger vascular adaptive responses. Among the various shear-induced signaling molecules, reactive oxygen species (ROS) and nitric oxide (NO) have been implicated in vascular homeostasis and diseases. In this review, we explore the molecular, cellular, and vascular processes arising from shear-induced signaling (mechanotransduction) with emphasis on the roles of ROS and NO, and also discuss the mechanisms that may lead to excessive vascular remodeling and thus drive pathobiologic processes responsible for atherosclerosis. Current evidence suggests that NADPH oxidase is one of main cellular sources of ROS generation in endothelial cells under flow condition. Flow patterns and magnitude of shear determine the amount of ROS produced by endothelial cells, usually an irregular flow pattern (disturbed or oscillatory) producing higher levels of ROS than a regular flow pattern (steady or pulsatile). ROS production is closely linked to NO generation and elevated levels of ROS lead to low NO bioavailability, as is often observed in endothelial cells exposed to irregular flow. The low NO bioavailability is partly caused by the reaction of ROS with NO to form peroxynitrite, a key molecule which may initiate many pro-atherogenic events. This differential production of ROS and RNS (reactive nitrogen species) under various flow patterns and conditions modulates endothelial gene expression and thus results in differential vascular responses. Moreover, ROS/RNS are able to promote specific post-translational modifications in regulatory proteins (including S-glutathionylation, S-nitrosylation and tyrosine nitration), which constitute chemical signals that are relevant in cardiovascular pathophysiology. Overall, the dynamic interplay between local hemodynamic milieu and the resulting oxidative and S-nitrosative modification of regulatory proteins is important for ensuing vascular homeostasis. Based on available evidence, it is proposed that a regular flow pattern produces lower levels of ROS and higher NO bioavailability, creating an anti-atherogenic environment. On the other hand, an irregular flow pattern results in higher levels of ROS and yet lower NO bioavailability, thus triggering pro-atherogenic effects. {\circledC} 2014 Hsieh et al.; licensee BioMed Central Ltd.",
keywords = "Endothelial cell, Flow pattern, Mechanotransduction, Nitric oxide (NO), Reactive oxygen species (ROS), Shear stress, calcium calmodulin dependent protein kinase II, calmodulin, endothelial leukocyte adhesion molecule 1, endothelial nitric oxide synthase, heme oxygenase 1, hydroxymethylglutaryl coenzyme A reductase kinase, immunoglobulin enhancer binding protein, intercellular adhesion molecule 1, kruppel like factor 2, messenger RNA, monocyte chemotactic protein 1, nitric oxide, oxidized low density lipoprotein, peroxynitrite, reactive nitrogen species, reactive oxygen metabolite, reduced nicotinamide adenine dinucleotide phosphate oxidase, regulator protein, superoxide, thioredoxin 1, thioredoxin reductase 1, transcription factor AP 1, transcription factor Nrf2, tyrosine, unclassified drug, uncoupled endothelial nitric oxide synthase, vascular cell adhesion molecule 1, xanthine oxidase, antioxidant responsive element, atherogenesis, blood vessel reactivity, cardiovascular disease, disease association, endothelial dysfunction, endothelium cell, enzyme activation, enzyme activity, enzyme phosphorylation, flow kinetics, gene expression regulation, hemodynamics, homeostasis, laminar flow, mechanotransduction, mitochondrial membrane potential, mitochondrial respiration, nitration, nitrosylation, oscillation, oxidation reduction reaction, oxidative phosphorylation, pathophysiology, priority journal, protein binding, protein expression, protein modification, protein processing, proton transport, pulsatile flow, review, s glutathionylation, s nitrosylation, shear stress, tyrosine nitration, vascular endothelium, genetics, human, mechanical stress, metabolism, oxidative stress, signal transduction, Hemodynamics, Humans, Mechanotransduction, Cellular, Nitric Oxide, Oxidative Stress, Protein Processing, Post-Translational, Reactive Nitrogen Species, Reactive Oxygen Species, Signal Transduction, Stress, Mechanical",
author = "Hsyue-Jen Hsieh and Ching-Ann Liu and Bin Huang and Anne-Hh Tseng and Danny-Ling Wang",
note = "被引用次數:28 Export Date: 28 March 2016 CODEN: JBCIE 通訊地址: Wang, D.L.; Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan; 電子郵件: lingwang@ibms.sinica.edu.tw 化學物質/CAS: calcium calmodulin dependent protein kinase II, 141467-21-2; endothelial leukocyte adhesion molecule 1, 128875-25-2; endothelial nitric oxide synthase, 503473-02-7; hydroxymethylglutaryl coenzyme A reductase kinase, 172522-01-9, 72060-32-3; intercellular adhesion molecule 1, 126547-89-5; nitric oxide, 10102-43-9; reduced nicotinamide adenine dinucleotide phosphate oxidase, 9032-22-8; superoxide, 11062-77-4; tyrosine, 16870-43-2, 55520-40-6, 60-18-4; xanthine oxidase, 9002-17-9 出資詳情: NSC100-2221-E-002-113-MY2, National Science Council Taiwan 出資詳情: NSC 99-2320-B-001-010-MY3, National Science Council Taiwan 參考文獻: Chiu, J.J., Chien, S., Effects of disturbed flow on vascular endothelium: Pathophysiological basis and clinical perspectives (2011) Physiol Rev, 91, pp. 327-387. , 10.1152/physrev.00047.2009 21248169; Berk, B.C., Atheroprotective signaling mechanisms activated by steady laminar flow in endothelial cells (2008) Circulation, 117, pp. 1082-1089. , 10.1161/CIRCULATIONAHA.107.720730 18299513; Davies, P.F., Flow-mediated endothelial mechanotransduction (1995) Physiol Rev, 75, pp. 519-560. , 7624393; Pan, S., Molecular mechanisms responsible for the atheroprotective effects of laminar shear stress (2009) Antioxid Redox Signal, 11, pp. 1669-1682. , 10.1089/ars.2009.2487 19309258; Chien, S., Mechanotransduction and endothelial cell homeostasis: The wisdom of the cell (2007) Am J Physiol Heart Circ Physiol, 292, pp. 81209-81224. , 17098825; Vanderlaan, P.A., Reardon, C.A., Getz, G.S., Site specificity of atherosclerosis: Site-selective responses to atherosclerotic modulators (2004) Arterioscler Thromb Vasc Biol, 24, pp. 12-22. , 10.1161/01.ATV.0000105054.43931.f0 14604830; Hahn, C., Schwartz, M.A., The role of cellular adaptation to mechanical forces in atherosclerosis (2008) Arterioscler Thromb Vasc Biol, 28, pp. 2101-2107. , 10.1161/ATVBAHA.108.165951 18787190; Birukov, K.G., Cyclic stretch, reactive oxygen species, and vascular remodeling (2009) Antioxid Redox Signal, 11, pp. 1651-1667. , 10.1089/ars.2008.2390 19186986; Matlung, H.L., Bakker, E.N., Vanbavel, E., Shear stress, reactive oxygen species, and arterial structure and function (2009) Antioxid Redox Signal, 11, pp. 1699-1709. , 10.1089/ars.2008.2408 19186981; Cai, H., Harrison, D.G., Endothelial dysfunction in cardiovascular diseases: The role of oxidant stress (2000) Circ Res, 87, pp. 840-844. , 10.1161/01.RES.87.10.840 11073878; Stocker, R., Keaney Jr., F.J., Role of oxidative modifications in atherosclerosis (2004) Physiol Rev, 84, pp. 1381-1478. , 10.1152/physrev.00047.2003 15383655; Villacorta, L., Chang, L., Salvatore, S.R., Ichikawa, T., Zhang, J., Petrovic-Djergovic, D., Jia, L., Chen, Y.E., Electrophilic nitro-fatty acids inhibit vascular inflammation by disrupting LPS-dependent TLR4 signalling in lipid rafts (2013) Cardiovasc Res, 98, pp. 116-124. , 10.1093/cvr/cvt002 23334216; Cui, T., Schopfer, F.J., Zhang, J., Chen, K., Ichikawa, T., Baker, P.R., Batthyany, C., Patel, R.P., Nitrated fatty acids: Endogenous anti-inflammatory signaling mediators (2006) J Biol Chem, 281, pp. 35686-35698. , 10.1074/jbc.M603357200 16887803; Hare, J.M., Stamler, J.S., NO/redox disequilibrium in the failing heart and cardiovascular system (2005) J Clin Invest, 115, pp. 509-517. , 15765132; Landmesser, U., Spiekermann, S., Dikalov, S., Tatge, H., Wilke, R., Kohler, C., Harrison, D.G., Drexler, H., Vascular oxidative stress and endothelial dysfunction in patients with chronic heart failure: Role of xanthine-oxidase and extracellular superoxide dismutase (2002) Circulation, 106, pp. 3073-3078. , 10.1161/01.CIR.0000041431.57222.AF 12473554; Landmesser, U., Spiekermann, S., Preuss, C., Sorrentino, S., Fischer, D., Manes, C., Mueller, M., Drexler, H., Angiotensin II induces endothelial xanthine oxidase activation: Role for endothelial dysfunction in patients with coronary disease (2007) Arterioscler Thromb Vasc Biol, 27, pp. 943-948. , 10.1161/01.ATV.0000258415.32883.bf 17234726; Lassegue, B., San Martin, A., Griendling, K.K., Biochemistry, physiology, and pathophysiology of NADPH oxidases in the cardiovascular system (2012) Circ Res, 110, pp. 1364-1390. , 10.1161/CIRCRESAHA.111.243972 22581922; De Keulenaer, G.W., Chappell, D.C., Ishizaka, N., Nerem, R.M., Alexander, R.W., Griendling, K.K., Oscillatory and steady laminar shear stress differentially affect human endothelial redox state: Role of a superoxide-producing NADH oxidase (1998) Circ Res, 82, pp. 1094-1101. , 10.1161/01.RES.82.10.1094 9622162; Hsieh, H.J., Cheng, C.C., Wu, S.T., Chiu, J.J., Wung, B.S., Wang, D.L., Increase of reactive oxygen species (ROS) in endothelial cells by shear flow and involvement of ROS in shear-induced c-fos expression (1998) J Cell Physiol, 175, pp. 156-162. , 10.1002/(SICI)1097-4652(199805)175:2<156: AID-JCP5>3.0.CO;2-N 9525474; Godbole, A.S., Lu, X., Guo, X., Kassab, G.S., NADPH oxidase has a directional response to shear stress (2009) Am J Physiol Heart Circ Physiol, 296, pp. 8152-8158. , 19011040; Takabe, W., Jen, N., Ai, L., Hamilton, R., Wang, S., Holmes, K., Dharbandi, F., Barr, M.L., Oscillatory shear stress induces mitochondrial superoxide production: Implication of NADPH oxidase and c-Jun NH2-terminal kinase signaling (2011) Antioxid Redox Signal, 15, pp. 1379-1388. , 10.1089/ars.2010.3645 20919940; Duerrschmidt, N., Stielow, C., Muller, G., Pagano, P.J., Morawietz, H., NO-mediated regulation of NAD(P)H oxidase by laminar shear stress in human endothelial cells (2006) J Physiol, 576, pp. 557-567. , 10.1113/jphysiol.2006.111070 16873416; Goettsch, C., Goettsch, W., Brux, M., Haschke, C., Brunssen, C., Muller, G., Bornstein, S.R., Morawietz, H., Arterial flow reduces oxidative stress via an antioxidant response element and Oct-1 binding site within the NADPH oxidase 4 promoter in endothelial cells (2011) Basic Res Cardiol, 106, pp. 551-561. , 10.1007/s00395-011-0170-3 21399967; Huang, A., Sun, D., Kaley, G., Koller, A., Superoxide released to high intra-arteriolar pressure reduces nitric oxide-mediated shear stress- and agonist-induced dilations (1998) Circ Res, 83, pp. 960-965. , 10.1161/01.RES.83.9.960 9797346; Sorescu, G.P., Song, H., Tressel, S.L., Hwang, J., Dikalov, S., Smith, D.A., Boyd, N.L., Jo, H., Bone morphogenic protein 4 produced in endothelial cells by oscillatory shear stress induces monocyte adhesion by stimulating reactive oxygen species production from a nox1-based NADPH oxidase (2004) Circ Res, 95, pp. 773-779. , 10.1161/01.RES.0000145728.22878.45 15388638; Ali, M.H., Pearlstein, D.P., Mathieu, C.E., Schumacker, P.T., Mitochondrial requirement for endothelial responses to cyclic strain: Implications for mechanotransduction (2004) Am J Physiol Lung Cell Mol Physiol, 287, pp. 12486-12496. , 10.1152/ajplung.00389.2003 15090367; Liu, Y., Zhao, H., Li, H., Kalyanaraman, B., Nicolosi, A.C., Gutterman, D.D., Mitochondrial sources of H2O2 generation play a key role in flow-mediated dilation in human coronary resistance arteries (2003) Circ Res, 93, pp. 573-580. , 10.1161/01.RES.0000091261.19387.AE 12919951; Han, Z., Chen, Y.R., Jones III, I.C., Meenakshisundaram, G., Zweier, J.L., Alevriadou, B.R., Shear-induced reactive nitrogen species inhibit mitochondrial respiratory complex activities in cultured vascular endothelial cells (2007) Am J Physiol Cell Physiol, 292, pp. 31103-31112. , 17020931; Doehner, W., Schoene, N., Rauchhaus, M., Leyva-Leon, F., Pavitt, D.V., Reaveley, D.A., Schuler, G., Hambrecht, R., Effects of xanthine oxidase inhibition with allopurinol on endothelial function and peripheral blood flow in hyperuricemic patients with chronic heart failure: Results from 2 placebo-controlled studies (2002) Circulation, 105, pp. 2619-2624. , 10.1161/01.CIR.0000017502.58595.ED 12045167; McNally, J.S., Davis, M.E., Giddens, D.P., Saha, A., Hwang, J., Dikalov, S., Jo, H., Harrison, D.G., Role of xanthine oxidoreductase and NAD(P)H oxidase in endothelial superoxide production in response to oscillatory shear stress (2003) Am J Physiol Heart Circ Physiol, 285, pp. 82290-82297. , 12958034; Thomas, S.R., Witting, P.K., Drummond, G.R., Redox control of endothelial function and dysfunction: Molecular mechanisms and therapeutic opportunities (2008) Antioxid Redox Signal, 10, pp. 1713-1765. , 10.1089/ars.2008.2027 18707220; Youn, J.Y., Gao, L., Cai, H., The p47phox- and NADPH oxidase organiser 1 (NOXO1)-dependent activation of NADPH oxidase 1 (NOX1) mediates endothelial nitric oxide synthase (eNOS) uncoupling and endothelial dysfunction in a streptozotocin-induced murine model of diabetes (2012) Diabetologia, 55, pp. 2069-2079. , 10.1007/s00125-012-2557-6 22549734; Dikalova, A.E., Gongora, M.C., Harrison, D.G., Lambeth, J.D., Dikalov, S., Griendling, K.K., Upregulation of Nox1 in vascular smooth muscle leads to impaired endothelium-dependent relaxation via eNOS uncoupling (2010) Am J Physiol Heart Circ Physiol, 299, pp. 8673-8679. , 10.1152/ajpheart.00242.2010 20639222; Yang, Y.M., Huang, A., Kaley, G., Sun, D., ENOS uncoupling and endothelial dysfunction in aged vessels (2009) Am J Physiol Heart Circ Physiol, 297, pp. 81829-81836. , 10.1152/ajpheart.00230.2009 19767531; Uematsu, M., Ohara, Y., Navas, J.P., Nishida, K., Murphy, T.J., Alexander, R.W., Nerem, R.M., Harrison, D.G., Regulation of endothelial cell nitric oxide synthase mRNA expression by shear stress (1995) Am J Physiol, 269, pp. 31371-31378. , 8572165; Sessa, W.C., ENOS at a glance (2004) J Cell Sci, 117, pp. 2427-2429. , 10.1242/jcs.01165 15159447; Boo, Y.C., Jo, H., Flow-dependent regulation of endothelial nitric oxide synthase: Role of protein kinases (2003) Am J Physiol Cell Physiol, 285, pp. 3499-3508. , 10.1152/ajpcell.00122.2003 12900384; Dimmeler, S., Fleming, I., Fisslthaler, B., Hermann, C., Busse, R., Zeiher, A.M., Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation (1999) Nature, 399, pp. 601-605. , 10.1038/21224 10376603; Boo, Y.C., Hwang, J., Sykes, M., Michell, B.J., Kemp, B.E., Lum, H., Jo, H., Shear stress stimulates phosphorylation of eNOS at Ser(635) by a protein kinase A-dependent mechanism (2002) Am J Physiol Heart Circ Physiol, 283, pp. 81819-81828. , 12384459; Roy, D., Belsham, D.D., Melatonin receptor activation regulates GnRH gene expression and secretion in GT1-7 GnRH neurons. Signal transduction mechanisms (2002) J Biol Chem, 277, pp. 251-258. , 11684691; Li, Y., Ouyang, J., Zheng, H., Yu, Z., Wang, B., The role of caveolae in shear stress-induced endothelial nitric-oxide synthase activation (2005) Sheng Wu Yi Xue Gong Cheng Xue Za Zhi, 22, pp. 1020-1023. , 16294744; Kumar, S., Sud, N., Fonseca, F.V., Hou, Y., Black, S.M., Shear stress stimulates nitric oxide signaling in pulmonary arterial endothelial cells via a reduction in catalase activity: Role of protein kinase C delta (2010) Am J Physiol Lung Cell Mol Physiol, 298, pp. 12105-12116. , 10.1152/ajplung.00290.2009 19897742; Chen, Z., Peng, I.C., Sun, W., Su, M.I., Hsu, P.H., Fu, Y., Zhu, Y., Shyy, J.Y., AMP-activated protein kinase functionally phosphorylates endothelial nitric oxide synthase Ser633 (2009) Circ Res, 104, pp. 496-505. , 10.1161/CIRCRESAHA.108.187567 19131647; Zhang, Y.J., Lee, T.S., Kolb, E.M., Sun, K., Lu, X., Sladek, F.M., Kassab, G.S., Shyy, J.Y.J., AMP-activated protein kinase is involved in endothelial NO synthase activation in response to shear stress (2006) Arterioscl Throm Vas, 26, pp. 1281-1287. , 10.1161/01.ATV.0000221230.08596.98; Mattagajasingh, I., Kim, C.S., Naqvi, A., Yamamori, T., Hoffman, T.A., Jung, S.B., Dericco, J., Irani, K., SIRT1 promotes endothelium-dependent vascular relaxation by activating endothelial nitric oxide synthase (2007) Proc Natl Acad Sci USA, 104, pp. 14855-14860. , 10.1073/pnas.0704329104 17785417; Chen, Z., Peng, I.C., Cui, X., Li, Y.S., Chien, S., Shyy, J.Y., Shear stress, SIRT1, and vascular homeostasis (2010) Proc Natl Acad Sci U S A, 107, pp. 10268-10273. , 10.1073/pnas.1003833107 20479254; Senbanerjee, S., Lin, Z.Y., Atkins, G.B., Greif, D.M., Rao, R.M., Kumar, A., Feinberg, M.W., Luscinskas, F.W., KLF2 is a novel transcriptional regulator of endothelial proinflammatory activation (2004) J Exp Med, 199, pp. 1305-1315. , 10.1084/jem.20031132 15136591; Dekker, R.J., Van Soest, S., Fontijn, R.D., Salamanca, S., De Groot, P.G., Vanbavel, E., Pannekoek, H., Horrevoets, A.J.G., Prolonged fluid shear stress induces a distinct set of endothelial cell genes, most specifically lung Kr{\"u}ppel-like factor (KLF2) (2002) Blood, 100, pp. 1689-1698. , 10.1182/blood-2002-01-0046 12176889; Wang, W.Y., Ha, C.H., Jhun, B.S., Wong, C., Jain, M.K., Jin, Z.G., Fluid shear stress stimulates phosphorylation-dependent nuclear export of HDAC5 and mediates expression of KLF2 and eNOS (2010) Blood, 115, pp. 2971-2979. , 10.1182/blood-2009-05-224824 20042720; Hsieh, C.Y., Hsiao, H.Y., Wu, W.Y., Liu, C.A., Tsai, Y.C., Chao, Y.J., Wang, D.L., Hsieh, H.J., Regulation of shear-induced nuclear translocation of the Nrf2 transcription factor in endothelial cells (2009) J Biomed Sci, 16; Takabe, W., Warabi, E., Noguchi, N., Anti-Atherogenic Effect of Laminar Shear Stress via Nrf2 Activation (2011) Antioxid Redox Sign, 15, pp. 1415-1426. , 10.1089/ars.2010.3433; Warabi, E., Takabe, W., Minami, T., Inoue, K., Itoh, K., Yamamoto, M., Ishii, T., Noguchi, N., Shear stress stabilizes NF-E2-related factor 2 and induces antioxidant genes in endothelial cells: Role of reactive oxygen/nitrogen species (2007) Free Radic Biol Med, 42, pp. 260-269. , 10.1016/j.freeradbiomed.2006.10.043 17189831; Frangos, J.A., Eskin, S.G., McIntire, L.V., Ives, C.L., Flow effects on prostacyclin production by cultured human endothelial cells (1985) Science, 227, pp. 1477-1479. , 10.1126/science.3883488 3883488; Chen, X.L., Varner, S.E., Rao, A.S., Grey, J.Y., Thomas, S., Cook, C.K., Wasserman, M.A., Kunsch, C., Laminar flow induction of antioxidant response element-mediated genes in endothelial cells - A novel anti-inflammatory mechanism (2003) J Biol Chem, 278, pp. 703-711. , 10.1074/jbc.M203161200 12370194; Inoue, N., Ramasamy, S., Fukai, T., Nerem, R.M., Harrison, D.G., Shear stress modulates expression of Cu/Zn superoxide dismutase in human aortic endothelial cells (1996) Circ Res, 79, pp. 32-37. , 10.1161/01.RES.79.1.32 8925565; Chiu, J.J., Wung, B.S., Shyy, J.Y., Hsieh, H.J., Wang, D.L., Reactive oxygen species are involved in shear stress-induced intercellular adhesion molecule-1 expression in endothelial cells (1997) Arterioscler Thromb Vasc Biol, 17, pp. 3570-3577. , 10.1161/01.ATV.17.12.3570 9437207; Hwang, J., Saha, A., Boo, Y.C., Sorescu, G.P., McNally, J.S., Holland, S.M., Dikalov, S., Jo, H., Oscillatory shear stress stimulates endothelial production of O2- from p47phox-dependent NAD(P)H oxidases, leading to monocyte adhesion (2003) J Biol Chem, 278, pp. 47291-47298. , 10.1074/jbc.M305150200 12958309; Mohan, S., Koyoma, K., Thangasamy, A., Nakano, H., Glickman, R.D., Mohan, N., Low shear stress preferentially enhances IKK activity through selective sources of ROS for persistent activation of NF-kappa B in endothelial cells (2007) Am J Physiol-Cell Ph, 292, pp. 3362-C371; White, S.J., Hayes, E.M., Lehoux, S., Jeremy, J.Y., Horrevoets, A.J., Newby, A.C., Characterization of the differential response of endothelial cells exposed to normal and elevated laminar shear stress (2011) J Cell Physiol, 226, pp. 2841-2848. , 10.1002/jcp.22629 21302282; Chin, L.K., Yu, J.Q., Fu, Y., Yu, T., Liu, A.Q., Luo, K.Q., Production of reactive oxygen species in endothelial cells under different pulsatile shear stresses and glucose concentrations (2011) Lab Chip, 11, pp. 1856-1863. , 10.1039/c0lc00651c 21373653; Dikalov, S., Griendling, K.K., Harrison, D.G., Measurement of reactive oxygen species in cardiovascular studies (2007) Hypertension, 49, pp. 717-727. , 10.1161/01.HYP.0000258594.87211.6b 17296874; Bao, X.P., Lu, C.Y., Frangos, J.A., Mechanism of temporal gradients in shear-induced ERK1/2 activation and proliferation in endothelial cells (2001) Am J Physiol-Heart C, 281, pp. 822-H29; Lehoux, S., Redox signalling in vascular responses to shear and stretch (2006) Cardiovasc Res, 71, pp. 269-279. , 10.1016/j.cardiores.2006.05.008 16780820; Frangos, J.A., Huang, T.Y., Clark, C.B., Steady shear and step changes in shear stimulate endothelium via independent mechanisms-superposition of transient and sustained nitric oxide production (1996) Biochem Biophys Res Commun, 224, pp. 660-665. , 10.1006/bbrc.1996.1081 8713104; Nigro, P., Abe, J., Berk, B.C., Flow shear stress and atherosclerosis: A matter of site specificity (2011) Antioxid Redox Signal, 15, pp. 1405-1414. , 10.1089/ars.2010.3679 21050140; Lu, X., Kassab, G.S., Nitric oxide is significantly reduced in ex vivo porcine arteries during reverse flow because of increased superoxide production (2004) J Physiol Lond, 561, pp. 575-582. , 10.1113/jphysiol.2004.075218 15579542; Hsiai, T.K., Hwang, J., Barr, M.L., Correa, A., Hamilton, R., Alavi, M., Rouhanizadeh, M., Hazen, S.L., Hemodynamics influences vascular peroxynitrite formation: Implication for low-density lipoprotein apo-B-100 nitration (2007) Free Radical Bio Med, 42, pp. 519-529. , 10.1016/j.freeradbiomed.2006.11.017; Chatterjee, S., Browning, E.A., Hong, N., Debolt, K., Sorokina, E.M., Liu, W., Birnbaum, M.J., Fisher, A.B., Membrane depolarization is the trigger for PI3K/Akt activation and leads to the generation of ROS (2012) Am J Physiol Heart Circ Physiol, 302, pp. 8105-8114. , 10.1152/ajpheart.00298.2011 22003059; Meng, T.C., Fukada, T., Tonks, N.K., Reversible oxidation and inactivation of protein tyrosine phosphatases in vivo (2002) Mol Cell, 9, pp. 387-399. , 10.1016/S1097-2765(02)00445-8 11864611; Kwon, J., Lee, S.R., Yang, K.S., Ahn, Y., Kim, Y.J., Stadtman, E.R., Rhee, S.G., Reversible oxidation and inactivation of the tumor suppressor PTEN in cells stimulated with peptide growth factors (2004) Proc Natl Acad Sci USA, 101, pp. 16419-16424. , 10.1073/pnas.0407396101 15534200; Andersen, J.N., Mortensen, O.H., Peters, G.H., Drake, P.G., Iversen, L.F., Olsen, O.H., Jansen, P.G., Moller, N.P.H., Structural and evolutionary relationships among protein tyrosine phosphatase domains (2001) Mol Cell Biol, 21, pp. 7117-7136. , 10.1128/MCB.21.21.7117-7136.2001 11585896; Rhee, S.G., Bae, Y.S., Lee, S.R., Kwon, J., Hydrogen peroxide: A key messenger that modulates protein phosphorylation through cysteine oxidation (2000) Sci STKE, 2000, pp. 16e1; Chen, Y.Y., Chu, H.M., Pan, K.T., Teng, C.H., Wang, D.L., Wang, A.H., Khoo, K.H., Meng, T.C., Cysteine S-nitrosylation protects protein-tyrosine phosphatase 1B against oxidation-induced permanent inactivation (2008) J Biol Chem, 283, pp. 35265-35272. , 10.1074/jbc.M805287200 18840608; Yu, C.X., Li, S., Whorton, A.R., Redox regulation of PTEN by S-nitrosothiols (2005) Mol Pharmacol, 68, pp. 847-854. , 15967877; Barrett, D.M., Black, S.M., Todor, H., Schmidt-Ullrich, R.K., Dawson, K.S., Mikkelsen, R.B., Inhibition of protein-tyrosine phosphatases by mild oxidative stresses is dependent on S-nitrosylation (2005) J Biol Chem, 280, pp. 14453-14461. , 10.1074/jbc.M411523200 15684422; Hsu, M.F., Meng, T.C., Enhancement of insulin responsiveness by nitric oxide-mediated inactivation of protein-tyrosine phosphatases (2010) J Biol Chem, 285, pp. 7919-7928. , 10.1074/jbc.M109.057513 20064934; Lerner-Marmarosh, N., Yoshizumi, M., Che, W.Y., Surapisitchat, J., Kawakatsu, H., Akaike, M., Ding, B., Abe, J., Inhibition of tumor necrosis factor-alpha-induced SHP-2 phosphatase activity by shear stress - A mechanism to reduce endothelial inflammation (2003) Arterioscl Throm Vas, 23, pp. 1775-1781. , 10.1161/01.ATV.0000094432.98445.36; Huang, B., Chen, S.C., Wang, D.L., Shear flow increases S-nitrosylation of proteins in endothelial cells (2009) Cardiovasc Res, 83, pp. 536-546. , 10.1093/cvr/cvp154 19447776; Huang, B., Liao, C.L., Lin, Y.P., Chen, S.C., Wang, D.L., S-nitrosoproteome in endothelial cells revealed by a modified biotin switch approach coupled with Western blot-based two-dimensional gel electrophoresis (2009) J Proteome Res, 8, pp. 4835-4843. , 10.1021/pr9005662 19673540; Wung, B.S., Cheng, J.J., Chao, Y.J., Hsieh, H.J., Wang, D.L., Modulation of Ras/Raf/extracellular signal-regulated kinase pathway by reactive oxygen species is involved in cyclic strain-induced early growth response-1 gene expression in endothelial cells (1999) Circ Res, 84, pp. 804-812. , 10.1161/01.RES.84.7.804 10205148; Fourquet, S., Guerois, R., Biard, D., Toledano, M.B., Activation of NRF2 by nitrosative agents and H2O2 involves KEAP1 disulfide formation (2010) J Biol Chem, 285, pp. 8463-8471. , 10.1074/jbc.M109.051714 20061377; Brigelius-Flohe, R., Flohe, L., Basic principles and emerging concepts in the redox control of transcription factors (2011) Antioxid Redox Signal, 15, pp. 2335-2381. , 10.1089/ars.2010.3534 21194351; Wung, B.S., Cheng, J.J., Hsieh, H.J., Shyy, Y.J., Wang, D.L., Cyclic strain-induced monocyte chemotactic protein-1 gene expression in endothelial cells involves reactive oxygen species activation of activator protein 1 (1997) Circ Res, 81, pp. 1-7. , 10.1161/01.RES.81.1.1 9201021; Chappell, D.C., Varner, S.E., Nerem, R.M., Medford, R.M., Alexander, R.W., Oscillatory shear stress stimulates adhesion molecule expression in cultured human endothelium (1998) Circ Res, 82, pp. 532-539. , 10.1161/01.RES.82.5.532 9529157; Chiu, J.J., Lee, P.L., Chen, C.N., Lee, C.I., Chang, S.F., Chen, L.J., Lien, S.C., Chien, S., Shear stress increases ICAM-1 and decreases VCAM-1 and E-selectin expressions induced by tumor necrosis factor-alpha in endothelial cells (2004) Arterioscler Thromb Vasc Biol, 24, pp. 73-79. , 10.1161/01.ATV.0000106321.63667.24 14615388; Chiu, J.J., Chen, L.J., Lee, P.L., Lee, C.I., Lo, L.W., Usami, S., Chien, S., Shear stress inhibits adhesion molecule expression in vascular endothelial cells induced by coculture with smooth muscle cells (2003) Blood, 101, pp. 2667-2674. , 10.1182/blood-2002-08-2560 12468429; Haddad, O., Chotard-Ghodsnia, R., Verdier, C., Duperray, A., Tumor cell/endothelial cell tight contact upregulates endothelial adhesion molecule expression mediated by NF kappa B: Differential role of the shear stress (2010) Exp Cell Res, 316, pp. 615-626. , 10.1016/j.yexcr.2009.11.015 19944683; Sucosky, P., Balachandran, K., Elhammali, A., Jo, H., Yoganathan, A.P., Altered shear stress stimulates upregulation of endothelial VCAM-1 and ICAM-1 in a BMP-4- and TGF-beta1-dependent pathway (2009) Arterioscler Thromb Vasc Biol, 29, pp. 254-260. , 10.1161/ATVBAHA.108.176347 19023092; Khan, B.V., Harrison, D.G., Olbrych, M.T., Alexander, R.W., Medford, R.M., Nitric oxide regulates vascular cell adhesion molecule 1 gene expression and redox-sensitive transcriptional events in human vascular endothelial cells (1996) Proc Natl Acad Sci USA, 93, pp. 9114-9119. , 10.1073/pnas.93.17.9114 8799163; Thom, S.R., Bhopale, V.M., Milovanova, T.N., Yang, M., Bogush, M., Thioredoxin reductase linked to cytoskeleton by focal adhesion kinase reverses actin S-nitrosylation and restores neutrophil beta(2) integrin function (2012) J Biol Chem, 287, pp. 30346-30357. , 10.1074/jbc.M112.355875 22778269; Isaac, J., Tarapore, P., Zhang, X., Lam, Y.W., Ho, S.M., Site-specific S-nitrosylation of integrin alpha6 increases the extent of prostate cancer cell migration by enhancing integrin beta1 association and weakening adherence to laminin-1 (2012) Biochemistry, 51, pp. 9689-9697. , 10.1021/bi3012324 23106339; Selemidis, S., Dusting, G.J., Peshavariya, H., Kemp-Harper, B.K., Drummond, G.R., Nitric oxide suppresses NADPH oxidase-dependent superoxide production by S-nitrosylation in human endothelial cells (2007) Cardiovasc Res, 75, pp. 349-358. , 10.1016/j.cardiores.2007.03.030 17568572; Liu, W.R., Nakamura, H., Shioji, K., Tanito, M., Oka, S., Ahsan, M.K., Son, A., Yodoi, Y., Thioredoxin-1 ameliorates myosin-induced autoimmune myocarditis by suppressing chemokine expressions and leukocyte chemotaxis in mice (2004) Circulation, 110, pp. 1276-1283. , 10.1161/01.CIR.0000141803.41217.B6 15337697; Haendeler, J., Hoffmann, J., Tischler, V., Berk, B.C., Zeiher, A.M., Dimmeler, S., Redox regulatory and anti-apoptotic functions of thioredoxin depend on S-nitrosylation at cysteine 69 (2002) Nat Cell Biol, 4, pp. 743-749. , 10.1038/ncb851 12244325; Hoffmann, J., Dimmeler, S., Haendeler, J., Shear stress increases the amount of S-nitrosylated molecules in endothelial cells: Important role for signal transduction (2003) Febs Lett, 551, pp. 153-158. , 10.1016/S0014-5793(03)00917-7 12965221; Hoffmann, J., Haendeler, J., Zeiher, A.M., Dimmeler, S., TNF alpha and oxLDL reduce protein S-nitrosylation in endothelial cells (2001) J Biol Chem, 276, pp. 41383-41387. , 10.1074/jbc.M107566200 11524431; Marshall, H.E., Merchant, K., Stamler, J.S., Nitrosation and oxidation in the regulation of gene expression (2000) Faseb Journal, 14, pp. 1889-1900. , 10.1096/fj.00.011rev 11023973; Xanthoudakis, S., Miao, G., Wang, F., Pan, Y.C.E., Curran, T., Redox Activation of Fos Jun DNA-Binding Activity Is Mediated by a DNA-Repair Enzyme (1992) Embo J, 11, pp. 3323-3335. , 1380454; Kumar, S., Sun, X.T., Wedgwood, S., Black, S.M., Hydrogen peroxide decreases endothelial nitric oxide synthase promoter activity through the inhibition of AP-1 activity (2008) Am J Physiol-Lung C, 295, pp. 12370-L377. , 10.1152/ajplung.90205.2008; Lima, B., Forrester, M.T., Hess, D.T., Stamler, J.S., S-Nitrosylation in cardiovascular signaling (2010) Circ Res, 106, pp. 633-646. , 10.1161/CIRCRESAHA.109.207381 20203313; Jaffrey, S.R., Erdjument-Bromage, H., Ferris, C.D., Tempst, P., Snyder, S.H., Protein S-nitrosylation: A physiological signal for neuronal nitric oxide (2001) Nat Cell Biol, 3, pp. 193-197. , 10.1038/35055104 11175752; Koek, W., Campos, P.S., France, C.P., Cheng, K., Rice, K.C., GHB- and baclofen-induced hypothermia in mice: Interactions with the GABA-B receptor positive modulator CGP7930, the GABA-B receptor antagonist CGP35348, and the NOS inhibitor L-NAME (2009) Faseb Journal, 23; Hess, D.T., Matsumoto, A., Kim, S.O., Marshall, H.E., Stamler, J.S., Protein S-nitrosylation: Purview and parameters (2005) Nat Rev Mol Cell Bio, 6, pp. 150-166. , 10.1038/nrm1569; Iwakiri, Y., Satoh, A., Chatterjee, S., Toomre, D.K., Chalouni, C.M., Fulton, D., Groszmann, R.J., Sessa, W.C., Nitric oxide synthase generates nitric oxide locally to regulate compartmentalized protein S-nitrosylation and protein trafficking (2006) Proc Natl Acad Sci USA, 103, pp. 19777-19782. , 10.1073/pnas.0605907103 17170139; Pi, X., Wu, Y., Ferguson III, E.J., Portbury, A.L., Patterson, C., SDF-1alpha stimulates JNK3 activity via eNOS-dependent nitrosylation of MKP7 to enhance endothelial migration (2009) Proc Natl Acad Sci USA, 106, pp. 5675-5680. , 10.1073/pnas.0809568106 19307591; Lai, Y.C., Pan, K.T., Chang, G.F., Hsu, C.H., Khoo, K.H., Hung, C.H., Jiang, Y.J., Meng, T.C., Nitrite-mediated S-nitrosylation of caspase-3 prevents hypoxia-induced endothelial barrier dysfunction (2011) Circ Res, 109, pp. 1375-1386. , 10.1161/CIRCRESAHA.111.256479 22021929; Thibeault, S., Rautureau, Y., Oubaha, M., Faubert, D., Wilkes, B.C., Delisle, C., Gratton, J.P., S-Nitrosylation of beta-Catenin by eNOS-Derived NO Promotes VEGF-Induced Endothelial Cell Permeability (2010) Mol Cell, 39, pp. 468-476. , 10.1016/j.molcel.2010.07.013 20705246; Wadham, C., Parker, A., Wang, L.J., Xia, P., High glucose attenuates protein S-nitrosylation in endothelial cells - Role of oxidative stress (2007) Diabetes, 56, pp. 2715-2721. , 10.2337/db06-1294 17704302; Santhanam, L., Lim, H.K., Lim, H.K., Miriel, V., Brown, T., Patel, M., Balanson, S., Irani, K., Inducible NO synthase-dependent S-nitrosylation and activation of arginase1 contribute to age-related endothelial dysfunction (2007) Circ Res, 101, pp. 692-702. , 10.1161/CIRCRESAHA.107.157727 17704205; Matsushita, K., Morrell, C.N., Cambien, B., Yang, S.X., Yamakuchi, M., Bao, C., Hara, M.R., O'Rourke, B., Nitric oxide regulates exocytosis by S-nitrosylation of N-ethylmaleimide-sensitive factor (2003) Cell, 115, pp. 139-150. , 10.1016/S0092-8674(03)00803-1 14567912; Kang-Decker, N., Cao, S., Chatterjee, S., Yao, J., Egan, L.J., Semela, D., Mukhopadhyay, D., Shah, V., Nitric oxide promotes endothelial cell survival signaling through S-nitrosylation and activation of dynamin-2 (2007) J Cell Sci, 120, pp. 492-501. , 10.1242/jcs.03361 17251380; Chen, Y.J., Ku, W.C., Lin, P.Y., Chou, H.C., Khoo, K.H., S-alkylating labeling strategy for site-specific identification of the s-nitrosoproteome (2010) J Proteome Res, 9, pp. 6417-6439. , 10.1021/pr100680a 20925432; Erwin, P.A., Mitchell, D.A., Sartoretto, J., Marletta, M.A., Michel, T., Subcellular targeting and differential S-nitrosylation of endothelial nitric-oxide synthase (2006) J Biol Chem, 281, pp. 151-157. , 10.1074/jbc.M510421200 16286475; Ravi, K., Brennan, L.A., Levic, S., Ross, P.A., Black, S.M., S-nitrosylation of endothelial nitric oxide synthase is associated with monomerization and decreased enzyme activity (2004) Proc Natl Acad Sci USA, 101, pp. 2619-2624. , 10.1073/pnas.0300464101 14983058; Erwin, P.A., Lin, A.J., Golan, D.E., Michel, T., Receptor-regulated dynamic S-nitrosylation of endothelial nitric-oxide synthase in vascular endothelial cells (2005) J Biol Chem, 280, pp. 19888-19894. , 10.1074/jbc.M413058200 15774480; Martinez-Ruiz, A., Villanueva, L., Gonzalez De Orduna, C., Lopez-Ferrer, D., Higueras, M.A., Tarin, C., Rodriguez-Crespo, I., Lamas, S., S-nitrosylation of Hsp90 promotes the inhibition of its ATPase and endothelial nitric oxide synthase regulatory activities (2005) Proc Natl Acad Sci USA, 102, pp. 8525-8530. , 10.1073/pnas.0407294102 15937123; Benhar, M., Forrester, M.T., Stamler, J.S., Protein denitrosylation: Enzymatic mechanisms and cellular functions (2009) Nat Rev Mol Cell Bio, 10, pp. 721-732; Ni, C.W., Hsieh, H.J., Chao, Y.J., Wang, D.L., Interleukin-6-induced JAK2/STAT3 signaling pathway in endothelial cells is suppressed by hemodynamic flow (2004) Am J Physiol-Cell Ph, 287, pp. 3771-C780. , 10.1152/ajpcell.00532.2003; Tsai, Y.C., Hsieh, H.J., Liao, F., Ni, C.W., Chao, Y.J., Hsieh, C.Y., Wang, D.L., Laminar flow attenuates interferon-induced inflammatory responses in endothelial cells (2007) Cardiovasc Res, 74, pp. 497-505. , 10.1016/j.cardiores.2007.02.030 17383622; Murphy, E., Kohr, M., Sun, J., Nguyen, T., Steenbergen, C., S-nitrosylation: A radical way to protect the heart (2012) J Mol Cell Cardiol, 52, pp. 568-577. , 10.1016/j.yjmcc.2011.08.021 21907718",
year = "2014",
doi = "10.1186/1423-0127-21-3",
language = "English",
volume = "21",
journal = "Journal of Biomedical Science",
issn = "1021-7770",
publisher = "BioMed Central",
number = "1",

}

TY - JOUR

T1 - Shear-induced endothelial mechanotransduction: The interplay between reactive oxygen species (ROS) and nitric oxide (NO) and the pathophysiological implications

AU - Hsieh, Hsyue-Jen

AU - Liu, Ching-Ann

AU - Huang, Bin

AU - Tseng, Anne-Hh

AU - Wang, Danny-Ling

N1 - 被引用次數:28 Export Date: 28 March 2016 CODEN: JBCIE 通訊地址: Wang, D.L.; Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan; 電子郵件: lingwang@ibms.sinica.edu.tw 化學物質/CAS: calcium calmodulin dependent protein kinase II, 141467-21-2; endothelial leukocyte adhesion molecule 1, 128875-25-2; endothelial nitric oxide synthase, 503473-02-7; hydroxymethylglutaryl coenzyme A reductase kinase, 172522-01-9, 72060-32-3; intercellular adhesion molecule 1, 126547-89-5; nitric oxide, 10102-43-9; reduced nicotinamide adenine dinucleotide phosphate oxidase, 9032-22-8; superoxide, 11062-77-4; tyrosine, 16870-43-2, 55520-40-6, 60-18-4; xanthine oxidase, 9002-17-9 出資詳情: NSC100-2221-E-002-113-MY2, National Science Council Taiwan 出資詳情: NSC 99-2320-B-001-010-MY3, National Science Council Taiwan 參考文獻: Chiu, J.J., Chien, S., Effects of disturbed flow on vascular endothelium: Pathophysiological basis and clinical perspectives (2011) Physiol Rev, 91, pp. 327-387. , 10.1152/physrev.00047.2009 21248169; Berk, B.C., Atheroprotective signaling mechanisms activated by steady laminar flow in endothelial cells (2008) Circulation, 117, pp. 1082-1089. , 10.1161/CIRCULATIONAHA.107.720730 18299513; Davies, P.F., Flow-mediated endothelial mechanotransduction (1995) Physiol Rev, 75, pp. 519-560. , 7624393; Pan, S., Molecular mechanisms responsible for the atheroprotective effects of laminar shear stress (2009) Antioxid Redox Signal, 11, pp. 1669-1682. , 10.1089/ars.2009.2487 19309258; Chien, S., Mechanotransduction and endothelial cell homeostasis: The wisdom of the cell (2007) Am J Physiol Heart Circ Physiol, 292, pp. 81209-81224. , 17098825; Vanderlaan, P.A., Reardon, C.A., Getz, G.S., Site specificity of atherosclerosis: Site-selective responses to atherosclerotic modulators (2004) Arterioscler Thromb Vasc Biol, 24, pp. 12-22. , 10.1161/01.ATV.0000105054.43931.f0 14604830; Hahn, C., Schwartz, M.A., The role of cellular adaptation to mechanical forces in atherosclerosis (2008) Arterioscler Thromb Vasc Biol, 28, pp. 2101-2107. , 10.1161/ATVBAHA.108.165951 18787190; Birukov, K.G., Cyclic stretch, reactive oxygen species, and vascular remodeling (2009) Antioxid Redox Signal, 11, pp. 1651-1667. , 10.1089/ars.2008.2390 19186986; Matlung, H.L., Bakker, E.N., Vanbavel, E., Shear stress, reactive oxygen species, and arterial structure and function (2009) Antioxid Redox Signal, 11, pp. 1699-1709. , 10.1089/ars.2008.2408 19186981; Cai, H., Harrison, D.G., Endothelial dysfunction in cardiovascular diseases: The role of oxidant stress (2000) Circ Res, 87, pp. 840-844. , 10.1161/01.RES.87.10.840 11073878; Stocker, R., Keaney Jr., F.J., Role of oxidative modifications in atherosclerosis (2004) Physiol Rev, 84, pp. 1381-1478. , 10.1152/physrev.00047.2003 15383655; Villacorta, L., Chang, L., Salvatore, S.R., Ichikawa, T., Zhang, J., Petrovic-Djergovic, D., Jia, L., Chen, Y.E., Electrophilic nitro-fatty acids inhibit vascular inflammation by disrupting LPS-dependent TLR4 signalling in lipid rafts (2013) Cardiovasc Res, 98, pp. 116-124. , 10.1093/cvr/cvt002 23334216; Cui, T., Schopfer, F.J., Zhang, J., Chen, K., Ichikawa, T., Baker, P.R., Batthyany, C., Patel, R.P., Nitrated fatty acids: Endogenous anti-inflammatory signaling mediators (2006) J Biol Chem, 281, pp. 35686-35698. , 10.1074/jbc.M603357200 16887803; Hare, J.M., Stamler, J.S., NO/redox disequilibrium in the failing heart and cardiovascular system (2005) J Clin Invest, 115, pp. 509-517. , 15765132; Landmesser, U., Spiekermann, S., Dikalov, S., Tatge, H., Wilke, R., Kohler, C., Harrison, D.G., Drexler, H., Vascular oxidative stress and endothelial dysfunction in patients with chronic heart failure: Role of xanthine-oxidase and extracellular superoxide dismutase (2002) Circulation, 106, pp. 3073-3078. , 10.1161/01.CIR.0000041431.57222.AF 12473554; Landmesser, U., Spiekermann, S., Preuss, C., Sorrentino, S., Fischer, D., Manes, C., Mueller, M., Drexler, H., Angiotensin II induces endothelial xanthine oxidase activation: Role for endothelial dysfunction in patients with coronary disease (2007) Arterioscler Thromb Vasc Biol, 27, pp. 943-948. , 10.1161/01.ATV.0000258415.32883.bf 17234726; Lassegue, B., San Martin, A., Griendling, K.K., Biochemistry, physiology, and pathophysiology of NADPH oxidases in the cardiovascular system (2012) Circ Res, 110, pp. 1364-1390. , 10.1161/CIRCRESAHA.111.243972 22581922; De Keulenaer, G.W., Chappell, D.C., Ishizaka, N., Nerem, R.M., Alexander, R.W., Griendling, K.K., Oscillatory and steady laminar shear stress differentially affect human endothelial redox state: Role of a superoxide-producing NADH oxidase (1998) Circ Res, 82, pp. 1094-1101. , 10.1161/01.RES.82.10.1094 9622162; Hsieh, H.J., Cheng, C.C., Wu, S.T., Chiu, J.J., Wung, B.S., Wang, D.L., Increase of reactive oxygen species (ROS) in endothelial cells by shear flow and involvement of ROS in shear-induced c-fos expression (1998) J Cell Physiol, 175, pp. 156-162. , 10.1002/(SICI)1097-4652(199805)175:2<156: AID-JCP5>3.0.CO;2-N 9525474; Godbole, A.S., Lu, X., Guo, X., Kassab, G.S., NADPH oxidase has a directional response to shear stress (2009) Am J Physiol Heart Circ Physiol, 296, pp. 8152-8158. , 19011040; Takabe, W., Jen, N., Ai, L., Hamilton, R., Wang, S., Holmes, K., Dharbandi, F., Barr, M.L., Oscillatory shear stress induces mitochondrial superoxide production: Implication of NADPH oxidase and c-Jun NH2-terminal kinase signaling (2011) Antioxid Redox Signal, 15, pp. 1379-1388. , 10.1089/ars.2010.3645 20919940; Duerrschmidt, N., Stielow, C., Muller, G., Pagano, P.J., Morawietz, H., NO-mediated regulation of NAD(P)H oxidase by laminar shear stress in human endothelial cells (2006) J Physiol, 576, pp. 557-567. , 10.1113/jphysiol.2006.111070 16873416; Goettsch, C., Goettsch, W., Brux, M., Haschke, C., Brunssen, C., Muller, G., Bornstein, S.R., Morawietz, H., Arterial flow reduces oxidative stress via an antioxidant response element and Oct-1 binding site within the NADPH oxidase 4 promoter in endothelial cells (2011) Basic Res Cardiol, 106, pp. 551-561. , 10.1007/s00395-011-0170-3 21399967; Huang, A., Sun, D., Kaley, G., Koller, A., Superoxide released to high intra-arteriolar pressure reduces nitric oxide-mediated shear stress- and agonist-induced dilations (1998) Circ Res, 83, pp. 960-965. , 10.1161/01.RES.83.9.960 9797346; Sorescu, G.P., Song, H., Tressel, S.L., Hwang, J., Dikalov, S., Smith, D.A., Boyd, N.L., Jo, H., Bone morphogenic protein 4 produced in endothelial cells by oscillatory shear stress induces monocyte adhesion by stimulating reactive oxygen species production from a nox1-based NADPH oxidase (2004) Circ Res, 95, pp. 773-779. , 10.1161/01.RES.0000145728.22878.45 15388638; Ali, M.H., Pearlstein, D.P., Mathieu, C.E., Schumacker, P.T., Mitochondrial requirement for endothelial responses to cyclic strain: Implications for mechanotransduction (2004) Am J Physiol Lung Cell Mol Physiol, 287, pp. 12486-12496. , 10.1152/ajplung.00389.2003 15090367; Liu, Y., Zhao, H., Li, H., Kalyanaraman, B., Nicolosi, A.C., Gutterman, D.D., Mitochondrial sources of H2O2 generation play a key role in flow-mediated dilation in human coronary resistance arteries (2003) Circ Res, 93, pp. 573-580. , 10.1161/01.RES.0000091261.19387.AE 12919951; Han, Z., Chen, Y.R., Jones III, I.C., Meenakshisundaram, G., Zweier, J.L., Alevriadou, B.R., Shear-induced reactive nitrogen species inhibit mitochondrial respiratory complex activities in cultured vascular endothelial cells (2007) Am J Physiol Cell Physiol, 292, pp. 31103-31112. , 17020931; Doehner, W., Schoene, N., Rauchhaus, M., Leyva-Leon, F., Pavitt, D.V., Reaveley, D.A., Schuler, G., Hambrecht, R., Effects of xanthine oxidase inhibition with allopurinol on endothelial function and peripheral blood flow in hyperuricemic patients with chronic heart failure: Results from 2 placebo-controlled studies (2002) Circulation, 105, pp. 2619-2624. , 10.1161/01.CIR.0000017502.58595.ED 12045167; McNally, J.S., Davis, M.E., Giddens, D.P., Saha, A., Hwang, J., Dikalov, S., Jo, H., Harrison, D.G., Role of xanthine oxidoreductase and NAD(P)H oxidase in endothelial superoxide production in response to oscillatory shear stress (2003) Am J Physiol Heart Circ Physiol, 285, pp. 82290-82297. , 12958034; Thomas, S.R., Witting, P.K., Drummond, G.R., Redox control of endothelial function and dysfunction: Molecular mechanisms and therapeutic opportunities (2008) Antioxid Redox Signal, 10, pp. 1713-1765. , 10.1089/ars.2008.2027 18707220; Youn, J.Y., Gao, L., Cai, H., The p47phox- and NADPH oxidase organiser 1 (NOXO1)-dependent activation of NADPH oxidase 1 (NOX1) mediates endothelial nitric oxide synthase (eNOS) uncoupling and endothelial dysfunction in a streptozotocin-induced murine model of diabetes (2012) Diabetologia, 55, pp. 2069-2079. , 10.1007/s00125-012-2557-6 22549734; Dikalova, A.E., Gongora, M.C., Harrison, D.G., Lambeth, J.D., Dikalov, S., Griendling, K.K., Upregulation of Nox1 in vascular smooth muscle leads to impaired endothelium-dependent relaxation via eNOS uncoupling (2010) Am J Physiol Heart Circ Physiol, 299, pp. 8673-8679. , 10.1152/ajpheart.00242.2010 20639222; Yang, Y.M., Huang, A., Kaley, G., Sun, D., ENOS uncoupling and endothelial dysfunction in aged vessels (2009) Am J Physiol Heart Circ Physiol, 297, pp. 81829-81836. , 10.1152/ajpheart.00230.2009 19767531; Uematsu, M., Ohara, Y., Navas, J.P., Nishida, K., Murphy, T.J., Alexander, R.W., Nerem, R.M., Harrison, D.G., Regulation of endothelial cell nitric oxide synthase mRNA expression by shear stress (1995) Am J Physiol, 269, pp. 31371-31378. , 8572165; Sessa, W.C., ENOS at a glance (2004) J Cell Sci, 117, pp. 2427-2429. , 10.1242/jcs.01165 15159447; Boo, Y.C., Jo, H., Flow-dependent regulation of endothelial nitric oxide synthase: Role of protein kinases (2003) Am J Physiol Cell Physiol, 285, pp. 3499-3508. , 10.1152/ajpcell.00122.2003 12900384; Dimmeler, S., Fleming, I., Fisslthaler, B., Hermann, C., Busse, R., Zeiher, A.M., Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation (1999) Nature, 399, pp. 601-605. , 10.1038/21224 10376603; Boo, Y.C., Hwang, J., Sykes, M., Michell, B.J., Kemp, B.E., Lum, H., Jo, H., Shear stress stimulates phosphorylation of eNOS at Ser(635) by a protein kinase A-dependent mechanism (2002) Am J Physiol Heart Circ Physiol, 283, pp. 81819-81828. , 12384459; Roy, D., Belsham, D.D., Melatonin receptor activation regulates GnRH gene expression and secretion in GT1-7 GnRH neurons. Signal transduction mechanisms (2002) J Biol Chem, 277, pp. 251-258. , 11684691; Li, Y., Ouyang, J., Zheng, H., Yu, Z., Wang, B., The role of caveolae in shear stress-induced endothelial nitric-oxide synthase activation (2005) Sheng Wu Yi Xue Gong Cheng Xue Za Zhi, 22, pp. 1020-1023. , 16294744; Kumar, S., Sud, N., Fonseca, F.V., Hou, Y., Black, S.M., Shear stress stimulates nitric oxide signaling in pulmonary arterial endothelial cells via a reduction in catalase activity: Role of protein kinase C delta (2010) Am J Physiol Lung Cell Mol Physiol, 298, pp. 12105-12116. , 10.1152/ajplung.00290.2009 19897742; Chen, Z., Peng, I.C., Sun, W., Su, M.I., Hsu, P.H., Fu, Y., Zhu, Y., Shyy, J.Y., AMP-activated protein kinase functionally phosphorylates endothelial nitric oxide synthase Ser633 (2009) Circ Res, 104, pp. 496-505. , 10.1161/CIRCRESAHA.108.187567 19131647; Zhang, Y.J., Lee, T.S., Kolb, E.M., Sun, K., Lu, X., Sladek, F.M., Kassab, G.S., Shyy, J.Y.J., AMP-activated protein kinase is involved in endothelial NO synthase activation in response to shear stress (2006) Arterioscl Throm Vas, 26, pp. 1281-1287. , 10.1161/01.ATV.0000221230.08596.98; Mattagajasingh, I., Kim, C.S., Naqvi, A., Yamamori, T., Hoffman, T.A., Jung, S.B., Dericco, J., Irani, K., SIRT1 promotes endothelium-dependent vascular relaxation by activating endothelial nitric oxide synthase (2007) Proc Natl Acad Sci USA, 104, pp. 14855-14860. , 10.1073/pnas.0704329104 17785417; Chen, Z., Peng, I.C., Cui, X., Li, Y.S., Chien, S., Shyy, J.Y., Shear stress, SIRT1, and vascular homeostasis (2010) Proc Natl Acad Sci U S A, 107, pp. 10268-10273. , 10.1073/pnas.1003833107 20479254; Senbanerjee, S., Lin, Z.Y., Atkins, G.B., Greif, D.M., Rao, R.M., Kumar, A., Feinberg, M.W., Luscinskas, F.W., KLF2 is a novel transcriptional regulator of endothelial proinflammatory activation (2004) J Exp Med, 199, pp. 1305-1315. , 10.1084/jem.20031132 15136591; Dekker, R.J., Van Soest, S., Fontijn, R.D., Salamanca, S., De Groot, P.G., Vanbavel, E., Pannekoek, H., Horrevoets, A.J.G., Prolonged fluid shear stress induces a distinct set of endothelial cell genes, most specifically lung Krüppel-like factor (KLF2) (2002) Blood, 100, pp. 1689-1698. , 10.1182/blood-2002-01-0046 12176889; Wang, W.Y., Ha, C.H., Jhun, B.S., Wong, C., Jain, M.K., Jin, Z.G., Fluid shear stress stimulates phosphorylation-dependent nuclear export of HDAC5 and mediates expression of KLF2 and eNOS (2010) Blood, 115, pp. 2971-2979. , 10.1182/blood-2009-05-224824 20042720; Hsieh, C.Y., Hsiao, H.Y., Wu, W.Y., Liu, C.A., Tsai, Y.C., Chao, Y.J., Wang, D.L., Hsieh, H.J., Regulation of shear-induced nuclear translocation of the Nrf2 transcription factor in endothelial cells (2009) J Biomed Sci, 16; Takabe, W., Warabi, E., Noguchi, N., Anti-Atherogenic Effect of Laminar Shear Stress via Nrf2 Activation (2011) Antioxid Redox Sign, 15, pp. 1415-1426. , 10.1089/ars.2010.3433; Warabi, E., Takabe, W., Minami, T., Inoue, K., Itoh, K., Yamamoto, M., Ishii, T., Noguchi, N., Shear stress stabilizes NF-E2-related factor 2 and induces antioxidant genes in endothelial cells: Role of reactive oxygen/nitrogen species (2007) Free Radic Biol Med, 42, pp. 260-269. , 10.1016/j.freeradbiomed.2006.10.043 17189831; Frangos, J.A., Eskin, S.G., McIntire, L.V., Ives, C.L., Flow effects on prostacyclin production by cultured human endothelial cells (1985) Science, 227, pp. 1477-1479. , 10.1126/science.3883488 3883488; Chen, X.L., Varner, S.E., Rao, A.S., Grey, J.Y., Thomas, S., Cook, C.K., Wasserman, M.A., Kunsch, C., Laminar flow induction of antioxidant response element-mediated genes in endothelial cells - A novel anti-inflammatory mechanism (2003) J Biol Chem, 278, pp. 703-711. , 10.1074/jbc.M203161200 12370194; Inoue, N., Ramasamy, S., Fukai, T., Nerem, R.M., Harrison, D.G., Shear stress modulates expression of Cu/Zn superoxide dismutase in human aortic endothelial cells (1996) Circ Res, 79, pp. 32-37. , 10.1161/01.RES.79.1.32 8925565; Chiu, J.J., Wung, B.S., Shyy, J.Y., Hsieh, H.J., Wang, D.L., Reactive oxygen species are involved in shear stress-induced intercellular adhesion molecule-1 expression in endothelial cells (1997) Arterioscler Thromb Vasc Biol, 17, pp. 3570-3577. , 10.1161/01.ATV.17.12.3570 9437207; Hwang, J., Saha, A., Boo, Y.C., Sorescu, G.P., McNally, J.S., Holland, S.M., Dikalov, S., Jo, H., Oscillatory shear stress stimulates endothelial production of O2- from p47phox-dependent NAD(P)H oxidases, leading to monocyte adhesion (2003) J Biol Chem, 278, pp. 47291-47298. , 10.1074/jbc.M305150200 12958309; Mohan, S., Koyoma, K., Thangasamy, A., Nakano, H., Glickman, R.D., Mohan, N., Low shear stress preferentially enhances IKK activity through selective sources of ROS for persistent activation of NF-kappa B in endothelial cells (2007) Am J Physiol-Cell Ph, 292, pp. 3362-C371; White, S.J., Hayes, E.M., Lehoux, S., Jeremy, J.Y., Horrevoets, A.J., Newby, A.C., Characterization of the differential response of endothelial cells exposed to normal and elevated laminar shear stress (2011) J Cell Physiol, 226, pp. 2841-2848. , 10.1002/jcp.22629 21302282; Chin, L.K., Yu, J.Q., Fu, Y., Yu, T., Liu, A.Q., Luo, K.Q., Production of reactive oxygen species in endothelial cells under different pulsatile shear stresses and glucose concentrations (2011) Lab Chip, 11, pp. 1856-1863. , 10.1039/c0lc00651c 21373653; Dikalov, S., Griendling, K.K., Harrison, D.G., Measurement of reactive oxygen species in cardiovascular studies (2007) Hypertension, 49, pp. 717-727. , 10.1161/01.HYP.0000258594.87211.6b 17296874; Bao, X.P., Lu, C.Y., Frangos, J.A., Mechanism of temporal gradients in shear-induced ERK1/2 activation and proliferation in endothelial cells (2001) Am J Physiol-Heart C, 281, pp. 822-H29; Lehoux, S., Redox signalling in vascular responses to shear and stretch (2006) Cardiovasc Res, 71, pp. 269-279. , 10.1016/j.cardiores.2006.05.008 16780820; Frangos, J.A., Huang, T.Y., Clark, C.B., Steady shear and step changes in shear stimulate endothelium via independent mechanisms-superposition of transient and sustained nitric oxide production (1996) Biochem Biophys Res Commun, 224, pp. 660-665. , 10.1006/bbrc.1996.1081 8713104; Nigro, P., Abe, J., Berk, B.C., Flow shear stress and atherosclerosis: A matter of site specificity (2011) Antioxid Redox Signal, 15, pp. 1405-1414. , 10.1089/ars.2010.3679 21050140; Lu, X., Kassab, G.S., Nitric oxide is significantly reduced in ex vivo porcine arteries during reverse flow because of increased superoxide production (2004) J Physiol Lond, 561, pp. 575-582. , 10.1113/jphysiol.2004.075218 15579542; Hsiai, T.K., Hwang, J., Barr, M.L., Correa, A., Hamilton, R., Alavi, M., Rouhanizadeh, M., Hazen, S.L., Hemodynamics influences vascular peroxynitrite formation: Implication for low-density lipoprotein apo-B-100 nitration (2007) Free Radical Bio Med, 42, pp. 519-529. , 10.1016/j.freeradbiomed.2006.11.017; Chatterjee, S., Browning, E.A., Hong, N., Debolt, K., Sorokina, E.M., Liu, W., Birnbaum, M.J., Fisher, A.B., Membrane depolarization is the trigger for PI3K/Akt activation and leads to the generation of ROS (2012) Am J Physiol Heart Circ Physiol, 302, pp. 8105-8114. , 10.1152/ajpheart.00298.2011 22003059; Meng, T.C., Fukada, T., Tonks, N.K., Reversible oxidation and inactivation of protein tyrosine phosphatases in vivo (2002) Mol Cell, 9, pp. 387-399. , 10.1016/S1097-2765(02)00445-8 11864611; Kwon, J., Lee, S.R., Yang, K.S., Ahn, Y., Kim, Y.J., Stadtman, E.R., Rhee, S.G., Reversible oxidation and inactivation of the tumor suppressor PTEN in cells stimulated with peptide growth factors (2004) Proc Natl Acad Sci USA, 101, pp. 16419-16424. , 10.1073/pnas.0407396101 15534200; Andersen, J.N., Mortensen, O.H., Peters, G.H., Drake, P.G., Iversen, L.F., Olsen, O.H., Jansen, P.G., Moller, N.P.H., Structural and evolutionary relationships among protein tyrosine phosphatase domains (2001) Mol Cell Biol, 21, pp. 7117-7136. , 10.1128/MCB.21.21.7117-7136.2001 11585896; Rhee, S.G., Bae, Y.S., Lee, S.R., Kwon, J., Hydrogen peroxide: A key messenger that modulates protein phosphorylation through cysteine oxidation (2000) Sci STKE, 2000, pp. 16e1; Chen, Y.Y., Chu, H.M., Pan, K.T., Teng, C.H., Wang, D.L., Wang, A.H., Khoo, K.H., Meng, T.C., Cysteine S-nitrosylation protects protein-tyrosine phosphatase 1B against oxidation-induced permanent inactivation (2008) J Biol Chem, 283, pp. 35265-35272. , 10.1074/jbc.M805287200 18840608; Yu, C.X., Li, S., Whorton, A.R., Redox regulation of PTEN by S-nitrosothiols (2005) Mol Pharmacol, 68, pp. 847-854. , 15967877; Barrett, D.M., Black, S.M., Todor, H., Schmidt-Ullrich, R.K., Dawson, K.S., Mikkelsen, R.B., Inhibition of protein-tyrosine phosphatases by mild oxidative stresses is dependent on S-nitrosylation (2005) J Biol Chem, 280, pp. 14453-14461. , 10.1074/jbc.M411523200 15684422; Hsu, M.F., Meng, T.C., Enhancement of insulin responsiveness by nitric oxide-mediated inactivation of protein-tyrosine phosphatases (2010) J Biol Chem, 285, pp. 7919-7928. , 10.1074/jbc.M109.057513 20064934; Lerner-Marmarosh, N., Yoshizumi, M., Che, W.Y., Surapisitchat, J., Kawakatsu, H., Akaike, M., Ding, B., Abe, J., Inhibition of tumor necrosis factor-alpha-induced SHP-2 phosphatase activity by shear stress - A mechanism to reduce endothelial inflammation (2003) Arterioscl Throm Vas, 23, pp. 1775-1781. , 10.1161/01.ATV.0000094432.98445.36; Huang, B., Chen, S.C., Wang, D.L., Shear flow increases S-nitrosylation of proteins in endothelial cells (2009) Cardiovasc Res, 83, pp. 536-546. , 10.1093/cvr/cvp154 19447776; Huang, B., Liao, C.L., Lin, Y.P., Chen, S.C., Wang, D.L., S-nitrosoproteome in endothelial cells revealed by a modified biotin switch approach coupled with Western blot-based two-dimensional gel electrophoresis (2009) J Proteome Res, 8, pp. 4835-4843. , 10.1021/pr9005662 19673540; Wung, B.S., Cheng, J.J., Chao, Y.J., Hsieh, H.J., Wang, D.L., Modulation of Ras/Raf/extracellular signal-regulated kinase pathway by reactive oxygen species is involved in cyclic strain-induced early growth response-1 gene expression in endothelial cells (1999) Circ Res, 84, pp. 804-812. , 10.1161/01.RES.84.7.804 10205148; Fourquet, S., Guerois, R., Biard, D., Toledano, M.B., Activation of NRF2 by nitrosative agents and H2O2 involves KEAP1 disulfide formation (2010) J Biol Chem, 285, pp. 8463-8471. , 10.1074/jbc.M109.051714 20061377; Brigelius-Flohe, R., Flohe, L., Basic principles and emerging concepts in the redox control of transcription factors (2011) Antioxid Redox Signal, 15, pp. 2335-2381. , 10.1089/ars.2010.3534 21194351; Wung, B.S., Cheng, J.J., Hsieh, H.J., Shyy, Y.J., Wang, D.L., Cyclic strain-induced monocyte chemotactic protein-1 gene expression in endothelial cells involves reactive oxygen species activation of activator protein 1 (1997) Circ Res, 81, pp. 1-7. , 10.1161/01.RES.81.1.1 9201021; Chappell, D.C., Varner, S.E., Nerem, R.M., Medford, R.M., Alexander, R.W., Oscillatory shear stress stimulates adhesion molecule expression in cultured human endothelium (1998) Circ Res, 82, pp. 532-539. , 10.1161/01.RES.82.5.532 9529157; Chiu, J.J., Lee, P.L., Chen, C.N., Lee, C.I., Chang, S.F., Chen, L.J., Lien, S.C., Chien, S., Shear stress increases ICAM-1 and decreases VCAM-1 and E-selectin expressions induced by tumor necrosis factor-alpha in endothelial cells (2004) Arterioscler Thromb Vasc Biol, 24, pp. 73-79. , 10.1161/01.ATV.0000106321.63667.24 14615388; Chiu, J.J., Chen, L.J., Lee, P.L., Lee, C.I., Lo, L.W., Usami, S., Chien, S., Shear stress inhibits adhesion molecule expression in vascular endothelial cells induced by coculture with smooth muscle cells (2003) Blood, 101, pp. 2667-2674. , 10.1182/blood-2002-08-2560 12468429; Haddad, O., Chotard-Ghodsnia, R., Verdier, C., Duperray, A., Tumor cell/endothelial cell tight contact upregulates endothelial adhesion molecule expression mediated by NF kappa B: Differential role of the shear stress (2010) Exp Cell Res, 316, pp. 615-626. , 10.1016/j.yexcr.2009.11.015 19944683; Sucosky, P., Balachandran, K., Elhammali, A., Jo, H., Yoganathan, A.P., Altered shear stress stimulates upregulation of endothelial VCAM-1 and ICAM-1 in a BMP-4- and TGF-beta1-dependent pathway (2009) Arterioscler Thromb Vasc Biol, 29, pp. 254-260. , 10.1161/ATVBAHA.108.176347 19023092; Khan, B.V., Harrison, D.G., Olbrych, M.T., Alexander, R.W., Medford, R.M., Nitric oxide regulates vascular cell adhesion molecule 1 gene expression and redox-sensitive transcriptional events in human vascular endothelial cells (1996) Proc Natl Acad Sci USA, 93, pp. 9114-9119. , 10.1073/pnas.93.17.9114 8799163; Thom, S.R., Bhopale, V.M., Milovanova, T.N., Yang, M., Bogush, M., Thioredoxin reductase linked to cytoskeleton by focal adhesion kinase reverses actin S-nitrosylation and restores neutrophil beta(2) integrin function (2012) J Biol Chem, 287, pp. 30346-30357. , 10.1074/jbc.M112.355875 22778269; Isaac, J., Tarapore, P., Zhang, X., Lam, Y.W., Ho, S.M., Site-specific S-nitrosylation of integrin alpha6 increases the extent of prostate cancer cell migration by enhancing integrin beta1 association and weakening adherence to laminin-1 (2012) Biochemistry, 51, pp. 9689-9697. , 10.1021/bi3012324 23106339; Selemidis, S., Dusting, G.J., Peshavariya, H., Kemp-Harper, B.K., Drummond, G.R., Nitric oxide suppresses NADPH oxidase-dependent superoxide production by S-nitrosylation in human endothelial cells (2007) Cardiovasc Res, 75, pp. 349-358. , 10.1016/j.cardiores.2007.03.030 17568572; Liu, W.R., Nakamura, H., Shioji, K., Tanito, M., Oka, S., Ahsan, M.K., Son, A., Yodoi, Y., Thioredoxin-1 ameliorates myosin-induced autoimmune myocarditis by suppressing chemokine expressions and leukocyte chemotaxis in mice (2004) Circulation, 110, pp. 1276-1283. , 10.1161/01.CIR.0000141803.41217.B6 15337697; Haendeler, J., Hoffmann, J., Tischler, V., Berk, B.C., Zeiher, A.M., Dimmeler, S., Redox regulatory and anti-apoptotic functions of thioredoxin depend on S-nitrosylation at cysteine 69 (2002) Nat Cell Biol, 4, pp. 743-749. , 10.1038/ncb851 12244325; Hoffmann, J., Dimmeler, S., Haendeler, J., Shear stress increases the amount of S-nitrosylated molecules in endothelial cells: Important role for signal transduction (2003) Febs Lett, 551, pp. 153-158. , 10.1016/S0014-5793(03)00917-7 12965221; Hoffmann, J., Haendeler, J., Zeiher, A.M., Dimmeler, S., TNF alpha and oxLDL reduce protein S-nitrosylation in endothelial cells (2001) J Biol Chem, 276, pp. 41383-41387. , 10.1074/jbc.M107566200 11524431; Marshall, H.E., Merchant, K., Stamler, J.S., Nitrosation and oxidation in the regulation of gene expression (2000) Faseb Journal, 14, pp. 1889-1900. , 10.1096/fj.00.011rev 11023973; Xanthoudakis, S., Miao, G., Wang, F., Pan, Y.C.E., Curran, T., Redox Activation of Fos Jun DNA-Binding Activity Is Mediated by a DNA-Repair Enzyme (1992) Embo J, 11, pp. 3323-3335. , 1380454; Kumar, S., Sun, X.T., Wedgwood, S., Black, S.M., Hydrogen peroxide decreases endothelial nitric oxide synthase promoter activity through the inhibition of AP-1 activity (2008) Am J Physiol-Lung C, 295, pp. 12370-L377. , 10.1152/ajplung.90205.2008; Lima, B., Forrester, M.T., Hess, D.T., Stamler, J.S., S-Nitrosylation in cardiovascular signaling (2010) Circ Res, 106, pp. 633-646. , 10.1161/CIRCRESAHA.109.207381 20203313; Jaffrey, S.R., Erdjument-Bromage, H., Ferris, C.D., Tempst, P., Snyder, S.H., Protein S-nitrosylation: A physiological signal for neuronal nitric oxide (2001) Nat Cell Biol, 3, pp. 193-197. , 10.1038/35055104 11175752; Koek, W., Campos, P.S., France, C.P., Cheng, K., Rice, K.C., GHB- and baclofen-induced hypothermia in mice: Interactions with the GABA-B receptor positive modulator CGP7930, the GABA-B receptor antagonist CGP35348, and the NOS inhibitor L-NAME (2009) Faseb Journal, 23; Hess, D.T., Matsumoto, A., Kim, S.O., Marshall, H.E., Stamler, J.S., Protein S-nitrosylation: Purview and parameters (2005) Nat Rev Mol Cell Bio, 6, pp. 150-166. , 10.1038/nrm1569; Iwakiri, Y., Satoh, A., Chatterjee, S., Toomre, D.K., Chalouni, C.M., Fulton, D., Groszmann, R.J., Sessa, W.C., Nitric oxide synthase generates nitric oxide locally to regulate compartmentalized protein S-nitrosylation and protein trafficking (2006) Proc Natl Acad Sci USA, 103, pp. 19777-19782. , 10.1073/pnas.0605907103 17170139; Pi, X., Wu, Y., Ferguson III, E.J., Portbury, A.L., Patterson, C., SDF-1alpha stimulates JNK3 activity via eNOS-dependent nitrosylation of MKP7 to enhance endothelial migration (2009) Proc Natl Acad Sci USA, 106, pp. 5675-5680. , 10.1073/pnas.0809568106 19307591; Lai, Y.C., Pan, K.T., Chang, G.F., Hsu, C.H., Khoo, K.H., Hung, C.H., Jiang, Y.J., Meng, T.C., Nitrite-mediated S-nitrosylation of caspase-3 prevents hypoxia-induced endothelial barrier dysfunction (2011) Circ Res, 109, pp. 1375-1386. , 10.1161/CIRCRESAHA.111.256479 22021929; Thibeault, S., Rautureau, Y., Oubaha, M., Faubert, D., Wilkes, B.C., Delisle, C., Gratton, J.P., S-Nitrosylation of beta-Catenin by eNOS-Derived NO Promotes VEGF-Induced Endothelial Cell Permeability (2010) Mol Cell, 39, pp. 468-476. , 10.1016/j.molcel.2010.07.013 20705246; Wadham, C., Parker, A., Wang, L.J., Xia, P., High glucose attenuates protein S-nitrosylation in endothelial cells - Role of oxidative stress (2007) Diabetes, 56, pp. 2715-2721. , 10.2337/db06-1294 17704302; Santhanam, L., Lim, H.K., Lim, H.K., Miriel, V., Brown, T., Patel, M., Balanson, S., Irani, K., Inducible NO synthase-dependent S-nitrosylation and activation of arginase1 contribute to age-related endothelial dysfunction (2007) Circ Res, 101, pp. 692-702. , 10.1161/CIRCRESAHA.107.157727 17704205; Matsushita, K., Morrell, C.N., Cambien, B., Yang, S.X., Yamakuchi, M., Bao, C., Hara, M.R., O'Rourke, B., Nitric oxide regulates exocytosis by S-nitrosylation of N-ethylmaleimide-sensitive factor (2003) Cell, 115, pp. 139-150. , 10.1016/S0092-8674(03)00803-1 14567912; Kang-Decker, N., Cao, S., Chatterjee, S., Yao, J., Egan, L.J., Semela, D., Mukhopadhyay, D., Shah, V., Nitric oxide promotes endothelial cell survival signaling through S-nitrosylation and activation of dynamin-2 (2007) J Cell Sci, 120, pp. 492-501. , 10.1242/jcs.03361 17251380; Chen, Y.J., Ku, W.C., Lin, P.Y., Chou, H.C., Khoo, K.H., S-alkylating labeling strategy for site-specific identification of the s-nitrosoproteome (2010) J Proteome Res, 9, pp. 6417-6439. , 10.1021/pr100680a 20925432; Erwin, P.A., Mitchell, D.A., Sartoretto, J., Marletta, M.A., Michel, T., Subcellular targeting and differential S-nitrosylation of endothelial nitric-oxide synthase (2006) J Biol Chem, 281, pp. 151-157. , 10.1074/jbc.M510421200 16286475; Ravi, K., Brennan, L.A., Levic, S., Ross, P.A., Black, S.M., S-nitrosylation of endothelial nitric oxide synthase is associated with monomerization and decreased enzyme activity (2004) Proc Natl Acad Sci USA, 101, pp. 2619-2624. , 10.1073/pnas.0300464101 14983058; Erwin, P.A., Lin, A.J., Golan, D.E., Michel, T., Receptor-regulated dynamic S-nitrosylation of endothelial nitric-oxide synthase in vascular endothelial cells (2005) J Biol Chem, 280, pp. 19888-19894. , 10.1074/jbc.M413058200 15774480; Martinez-Ruiz, A., Villanueva, L., Gonzalez De Orduna, C., Lopez-Ferrer, D., Higueras, M.A., Tarin, C., Rodriguez-Crespo, I., Lamas, S., S-nitrosylation of Hsp90 promotes the inhibition of its ATPase and endothelial nitric oxide synthase regulatory activities (2005) Proc Natl Acad Sci USA, 102, pp. 8525-8530. , 10.1073/pnas.0407294102 15937123; Benhar, M., Forrester, M.T., Stamler, J.S., Protein denitrosylation: Enzymatic mechanisms and cellular functions (2009) Nat Rev Mol Cell Bio, 10, pp. 721-732; Ni, C.W., Hsieh, H.J., Chao, Y.J., Wang, D.L., Interleukin-6-induced JAK2/STAT3 signaling pathway in endothelial cells is suppressed by hemodynamic flow (2004) Am J Physiol-Cell Ph, 287, pp. 3771-C780. , 10.1152/ajpcell.00532.2003; Tsai, Y.C., Hsieh, H.J., Liao, F., Ni, C.W., Chao, Y.J., Hsieh, C.Y., Wang, D.L., Laminar flow attenuates interferon-induced inflammatory responses in endothelial cells (2007) Cardiovasc Res, 74, pp. 497-505. , 10.1016/j.cardiores.2007.02.030 17383622; Murphy, E., Kohr, M., Sun, J., Nguyen, T., Steenbergen, C., S-nitrosylation: A radical way to protect the heart (2012) J Mol Cell Cardiol, 52, pp. 568-577. , 10.1016/j.yjmcc.2011.08.021 21907718

PY - 2014

Y1 - 2014

N2 - Hemodynamic shear stress, the blood flow-generated frictional force acting on the vascular endothelial cells, is essential for endothelial homeostasis under normal physiological conditions. Mechanosensors on endothelial cells detect shear stress and transduce it into biochemical signals to trigger vascular adaptive responses. Among the various shear-induced signaling molecules, reactive oxygen species (ROS) and nitric oxide (NO) have been implicated in vascular homeostasis and diseases. In this review, we explore the molecular, cellular, and vascular processes arising from shear-induced signaling (mechanotransduction) with emphasis on the roles of ROS and NO, and also discuss the mechanisms that may lead to excessive vascular remodeling and thus drive pathobiologic processes responsible for atherosclerosis. Current evidence suggests that NADPH oxidase is one of main cellular sources of ROS generation in endothelial cells under flow condition. Flow patterns and magnitude of shear determine the amount of ROS produced by endothelial cells, usually an irregular flow pattern (disturbed or oscillatory) producing higher levels of ROS than a regular flow pattern (steady or pulsatile). ROS production is closely linked to NO generation and elevated levels of ROS lead to low NO bioavailability, as is often observed in endothelial cells exposed to irregular flow. The low NO bioavailability is partly caused by the reaction of ROS with NO to form peroxynitrite, a key molecule which may initiate many pro-atherogenic events. This differential production of ROS and RNS (reactive nitrogen species) under various flow patterns and conditions modulates endothelial gene expression and thus results in differential vascular responses. Moreover, ROS/RNS are able to promote specific post-translational modifications in regulatory proteins (including S-glutathionylation, S-nitrosylation and tyrosine nitration), which constitute chemical signals that are relevant in cardiovascular pathophysiology. Overall, the dynamic interplay between local hemodynamic milieu and the resulting oxidative and S-nitrosative modification of regulatory proteins is important for ensuing vascular homeostasis. Based on available evidence, it is proposed that a regular flow pattern produces lower levels of ROS and higher NO bioavailability, creating an anti-atherogenic environment. On the other hand, an irregular flow pattern results in higher levels of ROS and yet lower NO bioavailability, thus triggering pro-atherogenic effects. © 2014 Hsieh et al.; licensee BioMed Central Ltd.

AB - Hemodynamic shear stress, the blood flow-generated frictional force acting on the vascular endothelial cells, is essential for endothelial homeostasis under normal physiological conditions. Mechanosensors on endothelial cells detect shear stress and transduce it into biochemical signals to trigger vascular adaptive responses. Among the various shear-induced signaling molecules, reactive oxygen species (ROS) and nitric oxide (NO) have been implicated in vascular homeostasis and diseases. In this review, we explore the molecular, cellular, and vascular processes arising from shear-induced signaling (mechanotransduction) with emphasis on the roles of ROS and NO, and also discuss the mechanisms that may lead to excessive vascular remodeling and thus drive pathobiologic processes responsible for atherosclerosis. Current evidence suggests that NADPH oxidase is one of main cellular sources of ROS generation in endothelial cells under flow condition. Flow patterns and magnitude of shear determine the amount of ROS produced by endothelial cells, usually an irregular flow pattern (disturbed or oscillatory) producing higher levels of ROS than a regular flow pattern (steady or pulsatile). ROS production is closely linked to NO generation and elevated levels of ROS lead to low NO bioavailability, as is often observed in endothelial cells exposed to irregular flow. The low NO bioavailability is partly caused by the reaction of ROS with NO to form peroxynitrite, a key molecule which may initiate many pro-atherogenic events. This differential production of ROS and RNS (reactive nitrogen species) under various flow patterns and conditions modulates endothelial gene expression and thus results in differential vascular responses. Moreover, ROS/RNS are able to promote specific post-translational modifications in regulatory proteins (including S-glutathionylation, S-nitrosylation and tyrosine nitration), which constitute chemical signals that are relevant in cardiovascular pathophysiology. Overall, the dynamic interplay between local hemodynamic milieu and the resulting oxidative and S-nitrosative modification of regulatory proteins is important for ensuing vascular homeostasis. Based on available evidence, it is proposed that a regular flow pattern produces lower levels of ROS and higher NO bioavailability, creating an anti-atherogenic environment. On the other hand, an irregular flow pattern results in higher levels of ROS and yet lower NO bioavailability, thus triggering pro-atherogenic effects. © 2014 Hsieh et al.; licensee BioMed Central Ltd.

KW - Endothelial cell

KW - Flow pattern

KW - Mechanotransduction

KW - Nitric oxide (NO)

KW - Reactive oxygen species (ROS)

KW - Shear stress

KW - calcium calmodulin dependent protein kinase II

KW - calmodulin

KW - endothelial leukocyte adhesion molecule 1

KW - endothelial nitric oxide synthase

KW - heme oxygenase 1

KW - hydroxymethylglutaryl coenzyme A reductase kinase

KW - immunoglobulin enhancer binding protein

KW - intercellular adhesion molecule 1

KW - kruppel like factor 2

KW - messenger RNA

KW - monocyte chemotactic protein 1

KW - nitric oxide

KW - oxidized low density lipoprotein

KW - peroxynitrite

KW - reactive nitrogen species

KW - reactive oxygen metabolite

KW - reduced nicotinamide adenine dinucleotide phosphate oxidase

KW - regulator protein

KW - superoxide

KW - thioredoxin 1

KW - thioredoxin reductase 1

KW - transcription factor AP 1

KW - transcription factor Nrf2

KW - tyrosine

KW - unclassified drug

KW - uncoupled endothelial nitric oxide synthase

KW - vascular cell adhesion molecule 1

KW - xanthine oxidase

KW - antioxidant responsive element

KW - atherogenesis

KW - blood vessel reactivity

KW - cardiovascular disease

KW - disease association

KW - endothelial dysfunction

KW - endothelium cell

KW - enzyme activation

KW - enzyme activity

KW - enzyme phosphorylation

KW - flow kinetics

KW - gene expression regulation

KW - hemodynamics

KW - homeostasis

KW - laminar flow

KW - mechanotransduction

KW - mitochondrial membrane potential

KW - mitochondrial respiration

KW - nitration

KW - nitrosylation

KW - oscillation

KW - oxidation reduction reaction

KW - oxidative phosphorylation

KW - pathophysiology

KW - priority journal

KW - protein binding

KW - protein expression

KW - protein modification

KW - protein processing

KW - proton transport

KW - pulsatile flow

KW - review

KW - s glutathionylation

KW - s nitrosylation

KW - shear stress

KW - tyrosine nitration

KW - vascular endothelium

KW - genetics

KW - human

KW - mechanical stress

KW - metabolism

KW - oxidative stress

KW - signal transduction

KW - Hemodynamics

KW - Humans

KW - Mechanotransduction, Cellular

KW - Nitric Oxide

KW - Oxidative Stress

KW - Protein Processing, Post-Translational

KW - Reactive Nitrogen Species

KW - Reactive Oxygen Species

KW - Signal Transduction

KW - Stress, Mechanical

U2 - 10.1186/1423-0127-21-3

DO - 10.1186/1423-0127-21-3

M3 - Article

VL - 21

JO - Journal of Biomedical Science

JF - Journal of Biomedical Science

SN - 1021-7770

IS - 1

ER -