In situ formation and scanning electrochemical microscopy assisted positioning of NO-sensors above human umbilical vein endothelial cells for the detection of nitric oxide release

2003 ◽  
Vol 5 (10) ◽  
pp. 847-852 ◽  
Author(s):  
Alain Pailleret ◽  
Joshua Oni ◽  
Sabine Reiter ◽  
Sonnur Isik ◽  
Mathieu Etienne ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Umbilical Vein ◽  
Scanning Electrochemical Microscopy ◽  
Human Umbilical Vein ◽  
Nitric Oxide Release ◽  
In Situ Formation ◽  
Umbilical Vein Endothelial Cells ◽  
Electrochemical Microscopy

Sesamol induces nitric oxide release from human umbilical vein endothelial cells

Lipids ◽  
2005 ◽  
Vol 40 (9) ◽  
pp. 955-961 ◽  
Author(s):  
Pey-Rong Chen ◽  
Chingmin E. Tsai ◽  
Hang Chang ◽  
Tsuei-Ling Liu ◽  
Chun-Chung Lee
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Nitric Oxide Release ◽  
Umbilical Vein Endothelial Cells

scholarly journals Effects of Propofol on Cyclic Strain-induced Endothelin-1 Expression in Human Umbilical Vein Endothelial Cells

2009 ◽  
Vol 110 (1) ◽  
pp. 74-80 ◽  
Author(s):  
Tzu-Hurng Cheng ◽  
Jin-Jer Chen ◽  
Cheng-Hsien Chen ◽  
Kar-Lok Wong
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Protein Kinase ◽  
Umbilical Vein ◽  
Cyclic Strain ◽  
Nitric Oxide Production ◽  
Human Umbilical Vein ◽  
Oxide Production ◽  
Extracellular Signal ◽  
Umbilical Vein Endothelial Cells

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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