MS163 IMPACT OF CIGARETTE SMOKE ON NO BIOAVAILABILITY IN ENDOTHELIAL CELLS: ROLE OF VASCULAR NADPH OXIDASE

2010 ◽  
Vol 11 (2) ◽  
pp. 142
Author(s):  
Y. Steffen
Keyword(s):  
Endothelial Cells ◽  
Nadph Oxidase ◽  
Cigarette Smoke ◽  
No Bioavailability

scholarly journals The Role of Vascular Endothelial Growth Factor-Induced Activation of NADPH Oxidase in Choroidal Endothelial Cells and Choroidal Neovascularization

2010 ◽  
Vol 177 (4) ◽  
pp. 2091-2102 ◽  
Author(s):  
Elizabeth Monaghan-Benson ◽  
John Hartmann ◽  
Aleksandr E. Vendrov ◽  
Steve Budd ◽  
Grace Byfield ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Nadph Oxidase ◽  
Choroidal Neovascularization ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Activation of endothelial cells after exposure to ambient ultrafine particles: The role of NADPH oxidase

2009 ◽  
Vol 236 (2) ◽  
pp. 183-193 ◽  
Author(s):  
Yiqun Mo ◽  
Rong Wan ◽  
Sufan Chien ◽  
David J. Tollerud ◽  
Qunwei Zhang
Keyword(s):  
Endothelial Cells ◽  
Nadph Oxidase ◽  
Ultrafine Particles

Replicative senescence promotes prothrombotic responses in endothelial cells: Role of NADPH oxidase- and cyclooxygenase-derived oxidative stress

2017 ◽  
Vol 93 ◽  
pp. 7-15 ◽  
Author(s):  
Grazielle Caroline Silva ◽  
Malak Abbas ◽  
Sonia Khemais-Benkhiat ◽  
Melanie Burban ◽  
Thais Porto Ribeiro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Nadph Oxidase ◽  
Replicative Senescence

Cigarette smoke extract inhibits angiogenesis of pulmonary artery endothelial cells: the role of calpain

2004 ◽  
Vol 287 (4) ◽  
pp. L794-L800 ◽  
Author(s):  
Yunchao Su ◽  
Wengang Cao ◽  
Zhaosheng Han ◽  
Edward R. Block
Keyword(s):  
Endothelial Cells ◽  
Cigarette Smoke ◽  
Wound Repair ◽  
Cigarette Smoke Extract ◽  
Tube Formation ◽  
Calpain Inhibitor ◽  
Endothelial Monolayer ◽  
Calpain Activity ◽  
Dose Dependent

Angiogenesis is an integral part of both the pulmonary inflammatory response to chronic exposure to cigarette smoke and the lung tissue remodeling associated with cigarette smoke-induced chronic obstructive pulmonary disease (COPD). To investigate the role of angiogenesis in the pathogenesis of COPD, we evaluated the effect of cigarette smoke extract (CSE) on angiogenesis of pulmonary artery endothelial cells (PAEC). Incubation of PAEC with 2.5–10% CSE resulted in a dose-dependent inhibition of endothelial monolayer wound repair. CSE also caused inhibition of tube formation on Matrigel, migration in a Boyden chamber, and proliferation of PAEC. Because calpain, a family of calcium-dependent intracellular proteases, mediates cytoskeletal signaling in endothelial motility, we explored the role of calpain in the CSE-induced inhibition of endothelial angiogenesis. Incubation of CSE resulted in a dose-dependent decrease in calpain activity. Calpain inhibitor-1, a specific inhibitor of calpain, potentiates inhibitory effect of CSE on the endothelial monolayer wound repair, tube formation, cell migration, and cell proliferation. Transfection of PAEC with antisense oligodeoxyribonucleotides of calpastatin, the major endogenous calpain inhibitor, prevented CSE-induced increase in calpastatin protein content and CSE-induced decreases in calpain activity. It also prevented CSE-induced decreases in monolayer wound repair, tube formation, and migration. These results suggest that CSE attenuates angiogenesis of PAEC and the mechanism involves inhibition of calpain. Impaired angiogenesis may impede the repair process in the lungs of cigarette smokers and contribute to the altered structural remodeling observed in the lungs of patients with cigarette smoke-related COPD.

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