Cigarette smoke extract induces HO-1 expression in mouse cerebral vascular endothelial cells

Involvement of c-Src/NADPH oxidase/PDGFR/JAK2/STAT3 pathway

Ruey Horng Shih, I-Ta Lee, Hsi Lung Hsieh, Yu Ru Kou, Chuen Mao Yang

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Several chemicals present in cigarette smoke (CS) have been reported to induce heme oxygenase-1 (HO-1) expression, which represents a prime defense mechanism in protecting the cells from stress-dependent adverse effects on peripheral vascular system. However, the effects of cigarette smoke extract (CSE) on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in brain vessels are not completely understood. Here, we used a mouse brain endothelial cell culture (bEnd.3) to investigate the effect of CSE on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in cerebral vessels. We demonstrated that sublethal concentrations of CSE (30-μg/ml) induced submaximal HO-1 expression in bEnd.3 cells. NADPH oxidase-dependent ROS generation played a key role in CSE-induced HO-1 expression. CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was observed by pretreatment with the respective pharmacological inhibitors or transfection with PDGFR shRNA. CSE activated NADPH oxidase through c-Src in bEnd.3 cells. Taken together, these results suggested that, in bEnd.3 cells, CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was regulated by c-Src or c-Src activated-NADPH oxidase/ROS.

Original languageEnglish
Pages (from-to)741-750
Number of pages10
JournalJournal of Cellular Physiology
Volume225
Issue number3
DOIs
Publication statusPublished - Dec 1 2010
Externally publishedYes

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Heme Oxygenase-1
NADPH Oxidase
Endothelial cells
Smoke
Tobacco Products
Endothelial Cells
Brain
Cell culture
Small Interfering RNA
Transfection
Blood Vessels
Cell Culture Techniques
Pharmacology

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

Cite this

Cigarette smoke extract induces HO-1 expression in mouse cerebral vascular endothelial cells : Involvement of c-Src/NADPH oxidase/PDGFR/JAK2/STAT3 pathway. / Shih, Ruey Horng; Lee, I-Ta; Hsieh, Hsi Lung; Kou, Yu Ru; Yang, Chuen Mao.

In: Journal of Cellular Physiology, Vol. 225, No. 3, 01.12.2010, p. 741-750.

Research output: Contribution to journalArticle

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abstract = "Several chemicals present in cigarette smoke (CS) have been reported to induce heme oxygenase-1 (HO-1) expression, which represents a prime defense mechanism in protecting the cells from stress-dependent adverse effects on peripheral vascular system. However, the effects of cigarette smoke extract (CSE) on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in brain vessels are not completely understood. Here, we used a mouse brain endothelial cell culture (bEnd.3) to investigate the effect of CSE on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in cerebral vessels. We demonstrated that sublethal concentrations of CSE (30-μg/ml) induced submaximal HO-1 expression in bEnd.3 cells. NADPH oxidase-dependent ROS generation played a key role in CSE-induced HO-1 expression. CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was observed by pretreatment with the respective pharmacological inhibitors or transfection with PDGFR shRNA. CSE activated NADPH oxidase through c-Src in bEnd.3 cells. Taken together, these results suggested that, in bEnd.3 cells, CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was regulated by c-Src or c-Src activated-NADPH oxidase/ROS.",
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