scholarly journals Proteomic Analysis of Vascular Endothelial Cells-Effects of Laminar Shear Stress and High Glucose

2009 ◽  
Vol 02 (10) ◽  
pp. 445-454 ◽  
Author(s):  
Xiao-Li Wang ◽  
Alex Fu ◽  
Craig Spiro ◽  
Hon-Chi Lee
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
High Glucose ◽  
Proteomic Analysis ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Laminar Shear Stress ◽  
Laminar Shear

Proteomic analysis of vascular endothelial cells in response to laminar shear stress

PROTEOMICS ◽  
2007 ◽  
Vol 7 (4) ◽  
pp. 588-596 ◽  
Author(s):  
Xiao-Li Wang ◽  
Alex Fu ◽  
Sreekumar Raghavakaimal ◽  
Hon-Chi Lee
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Proteomic Analysis ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Laminar Shear Stress ◽  
Laminar Shear

Shear-induced reactive nitrogen species inhibit mitochondrial respiratory complex activities in cultured vascular endothelial cells

2007 ◽  
Vol 292 (3) ◽  
pp. C1103-C1112 ◽  
Author(s):  
Zhaosheng Han ◽  
Yeong-Renn Chen ◽  
Charles I. Jones ◽  
Guruguhan Meenakshisundaram ◽  
Jay L. Zweier ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Reactive Nitrogen Species ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Nitrogen Species ◽  
Laminar Shear Stress ◽  
Steady Laminar Shear Stress ◽  
Laminar Shear ◽  
Steady Laminar

There is evidence that nitric oxide (NO), superoxide (O2•−), and their associated reactive nitrogen species (RNS) produced by vascular endothelial cells (ECs) in response to hemodynamic forces play a role in cell signaling. NO is known to impair mitochondrial respiration. We sought to determine whether exposure of human umbilical vein ECs (HUVECs) to steady laminar shear stress and the resultant NO production modulate electron transport chain (ETC) enzymatic activities. The activities of respiratory complexes I, II/III, and IV were dependent on the presence of serum and growth factor supplement in the medium. EC exposure to steady laminar shear stress (10 dyn/cm2) resulted in a gradual inhibition of each of the complexes starting as early as 5 min from the flow onset and lasting up to 16 h. Ramp flow resulted in inhibition of the complexes similar to that of step flow. When ECs were sheared in the presence of the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME; 100 μM), the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO; 100 μM), or the peroxynitrite (ONOO−) scavenger uric acid (UA; 50 μM), the flow-inhibitory effect on mitochondrial complexes was attenuated. In particular, l-NAME and UA abolished the flow effect on complex IV. Increased tyrosine nitration was observed in the mitochondria of sheared ECs, and UA blocked the shear-induced nitrotyrosine staining. In summary, shear stress induces mitochondrial RNS formation that inhibits the electron flux of the ETC at multiple sites. This may be a critical mechanism by which shear stress modulates EC signaling and function.

scholarly journals Functional lipidomics of vascular endothelial cells in response to laminar shear stress

2021 ◽  
Vol 35 (2) ◽  
Author(s):  
Tsuyoshi Hirata ◽  
Kimiko Yamamoto ◽  
Kazutaka Ikeda ◽  
Makoto Arita
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Laminar Shear Stress ◽  
Laminar Shear

scholarly journals Laminar Shear Stress Regulates Liver X Receptor in Vascular Endothelial Cells

2008 ◽  
Vol 28 (3) ◽  
pp. 527-533 ◽  
Author(s):  
Minjia Zhu ◽  
Yi Fu ◽  
Yingjian Hou ◽  
Nanping Wang ◽  
Youfei Guan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Vascular Endothelial Cells ◽  
Liver X Receptor ◽  
Vascular Endothelial ◽  
Laminar Shear Stress ◽  
Laminar Shear
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