Acrolein produces nitric oxide through the elevation of intracellular calcium levels to induce apoptosis in human umbilical vein endothelial cells: Implications for smoke angiopathy

Nitric Oxide ◽  
2006 ◽  
Vol 14 (2) ◽  
pp. 180-187 ◽  
Author(s):  
Yoshiko Misonou ◽  
Michio Asahi ◽  
Shunichi Yokoe ◽  
Eiji Miyoshi ◽  
Naoyuki Taniguchi
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Intracellular Calcium ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
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.

Tetrahydrobiopterin correctsEscherichia coliendotoxin-induced endothelial dysfunction

2005 ◽  
Vol 289 (4) ◽  
pp. H1752-H1757 ◽  
Author(s):  
Friedrich Mittermayer ◽  
Johannes Pleiner ◽  
Georg Schaller ◽  
Stefan Zorn ◽  
Khodadad Namiranian ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Vitamin C ◽  
Acute Inflammation ◽  
Umbilical Vein ◽  
Oxidant Stress ◽  
Double Blind ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Acute inflammation causes endothelial dysfunction, which is partly mediated by oxidant stress and inactivation of nitric oxide. The contribution of depletion of tetrahydrobiopterin (BH4), the cofactor required for nitric oxide generation, is unclear. In this randomized, double-blind, three-way crossover study, forearm blood flow (FBF) responses to ACh and glyceryltrinitrate (GTN) were measured before and 3.5 h after infusion of Escherichia coli endotoxin (LPS, 20 IU/kg iv) in eight healthy men. The effect of intra-arterial BH4(500 μg/min), placebo, or vitamin C (24 mg/min) was studied on separate days 3.5 h after LPS infusion. In addition, human umbilical vein endothelial cells were incubated for 24 h with vitamin C and LPS. ACh and GTN caused dose-dependent forearm vasodilation. The FBF response to ACh, which was decreased by 23 ± 17% ( P < 0.05) by LPS infusion, was restored to baseline reactivity by BH4and vitamin C. FBF responses to GTN were not affected by BH4or vitamin C. LPS increased leukocyte count, high-sensitivity C-reactive protein, IL-6, IL-1β, IFN-γ, monocyte chemoattractant protein-1, pulse rate, and body temperature and decreased platelet count and vitamin C concentration. Vitamin C increased forearm plasma concentration of BH4by 32% ( P < 0.02). Incubation with LPS and vitamin C, but not LPS alone, increased intracellular BH4concentration in human umbilical vein endothelial cells. Impaired endothelial function during acute inflammation can be restored by BH4or vitamin C. Vitamin C may exert some of its salutary effects by increasing BH4concentration.

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