p38 Mitogen-Activated Protein Kinase and Extracellular Signal-Regulated Kinase Regulate Nitric Oxide Production and Inflammatory Cytokine Expression in Raw Cells

2005 ◽  
Vol 5 (1) ◽  
pp. 30
Author(s):  
Cheol-Hee Choi ◽  
Sang-Hyun Kim
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase ◽  
Inflammatory Cytokine ◽  
Cytokine Expression ◽  
Mitogen Activated Protein Kinase ◽  
Nitric Oxide Production ◽  
Extracellular Signal Regulated Kinase ◽  
Oxide Production ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

Hypoxia induces nitric oxide production in mouse microglia via p38 mitogen-activated protein kinase pathway

2002 ◽  
Vol 107 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Sun Young Park ◽  
Heasuk Lee ◽  
Jinyoung Hur ◽  
Sun Yeou Kim ◽  
Hocheol Kim ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase ◽  
Mitogen Activated Protein Kinase ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Mitogen Activated Protein ◽  
Kinase Pathway

MEK5/ERK5: Mitogen-Activated Protein Kinase 5/Extracellular Signal-Regulated Kinase 5

2012 ◽  
pp. 1074-1074
Author(s):  
Andreas Gewies ◽  
Jürgen Ruland ◽  
Alexey Kotlyarov ◽  
Matthias Gaestel ◽  
Shiri Procaccia ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Mitogen Activated Protein Kinase ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

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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