Effects of propofol on cyclic strain-induced endothelin-1 expression in human umbilical vein endothelial cells

Tzu-Hurng Cheng, Jin Jer Chen, Cheng Hsien Chen, Kar Lok Wong

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

BACKGROUND: Propofol is one of the most popular intravenous induction agents of general anesthesia. Experimental results revealed that propofol exerted hypotensive and antioxidative effects. However, the intracellular mechanism of propofol remains to be delineated. The aims of this study were to test the hypothesis that propofol may alter strain-induced endothelin-1 (ET-1) secretion and nitric oxide production, and to identify the putative underlying signaling pathways in human umbilical vein endothelial cells. METHODS: Cultured human umbilical vein endothelial cells were exposed to cyclic strain in the presence of propofol, and ET-1 expression was examined by Northern blotting and enzyme-linked immunosorbent assay kit. Activation of extracellular signal-regulated protein kinase, endothelial nitric oxide synthase, and protein kinase B were assessed by Western blot analysis. RESULTS: The authors show that propofol inhibits strain-induced ET-1 expression, strain-increased reactive oxygen species formation, and extracellular signal-regulated protein kinase phosphorylation. On the contrary, nitric oxide production, endothelial nitric oxide synthase activity, and protein kinase B phosphorylation were enhanced by propofol treatment. Furthermore, in the presence of PTIO, a nitric oxide scavenger, and KT5823, a specific inhibitor of cyclic guanosine monophosphate-dependent protein kinase, the inhibitory effect of propofol on strain-induced extracellular signal-regulated protein kinase phosphorylation and ET-1 release was reversed. CONCLUSIONS: The authors demonstrate for the first time that propofol inhibits strain-induced ET-1 secretion and enhances strain-increased nitric oxide production in human umbilical vein endothelial cells. Thus, this study delivers important new insight into the molecular pathways that may contribute to the proposed hypotensive effects of propofol in the cardiovascular system.

Original languageEnglish
Pages (from-to)74-80
Number of pages7
JournalAnesthesiology
Volume110
Issue number1
DOIs
Publication statusPublished - Jan 2009

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Human Umbilical Vein Endothelial Cells
Endothelin-1
Propofol
Extracellular Signal-Regulated MAP Kinases
Nitric Oxide
Protein Kinases
Proto-Oncogene Proteins c-akt
Nitric Oxide Synthase Type III
Phosphorylation
Cyclic GMP-Dependent Protein Kinases
Cardiovascular System
Northern Blotting
General Anesthesia
Reactive Oxygen Species
Western Blotting
Enzyme-Linked Immunosorbent Assay

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Effects of propofol on cyclic strain-induced endothelin-1 expression in human umbilical vein endothelial cells. / Cheng, Tzu-Hurng; Chen, Jin Jer; Chen, Cheng Hsien; Wong, Kar Lok.

In: Anesthesiology, Vol. 110, No. 1, 01.2009, p. 74-80.

Research output: Contribution to journalArticle

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AB - BACKGROUND: Propofol is one of the most popular intravenous induction agents of general anesthesia. Experimental results revealed that propofol exerted hypotensive and antioxidative effects. However, the intracellular mechanism of propofol remains to be delineated. The aims of this study were to test the hypothesis that propofol may alter strain-induced endothelin-1 (ET-1) secretion and nitric oxide production, and to identify the putative underlying signaling pathways in human umbilical vein endothelial cells. METHODS: Cultured human umbilical vein endothelial cells were exposed to cyclic strain in the presence of propofol, and ET-1 expression was examined by Northern blotting and enzyme-linked immunosorbent assay kit. Activation of extracellular signal-regulated protein kinase, endothelial nitric oxide synthase, and protein kinase B were assessed by Western blot analysis. RESULTS: The authors show that propofol inhibits strain-induced ET-1 expression, strain-increased reactive oxygen species formation, and extracellular signal-regulated protein kinase phosphorylation. On the contrary, nitric oxide production, endothelial nitric oxide synthase activity, and protein kinase B phosphorylation were enhanced by propofol treatment. Furthermore, in the presence of PTIO, a nitric oxide scavenger, and KT5823, a specific inhibitor of cyclic guanosine monophosphate-dependent protein kinase, the inhibitory effect of propofol on strain-induced extracellular signal-regulated protein kinase phosphorylation and ET-1 release was reversed. CONCLUSIONS: The authors demonstrate for the first time that propofol inhibits strain-induced ET-1 secretion and enhances strain-increased nitric oxide production in human umbilical vein endothelial cells. Thus, this study delivers important new insight into the molecular pathways that may contribute to the proposed hypotensive effects of propofol in the cardiovascular system.

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