scholarly journals Characterization of the differential response of endothelial cells exposed to normal and elevated laminar shear stress

2011 ◽  
Vol 226 (11) ◽  
pp. 2841-2848 ◽  
Author(s):  
Stephen J. White ◽  
Elaine M. Hayes ◽  
Stéphanie Lehoux ◽  
Jamie Y. Jeremy ◽  
Anton J.G. Horrevoets ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Differential Response ◽  
Laminar Shear Stress ◽  
Laminar Shear

scholarly journals A Parallel-Plate Flow Chamber for Mechanical Characterization of Endothelial Cells Exposed to Laminar Shear Stress

2015 ◽  
Vol 9 (1) ◽  
pp. 127-138 ◽  
Author(s):  
Andrew K. Wong ◽  
Pierre LLanos ◽  
Nickolas Boroda ◽  
Seth R. Rosenberg ◽  
Sina Y. Rabbany
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Parallel Plate ◽  
Mechanical Characterization ◽  
Flow Chamber ◽  
Laminar Shear Stress ◽  
Parallel Plate Flow Chamber ◽  
Laminar Shear

scholarly journals Primary cilia of human endothelial cells disassemble under laminar shear stress

2004 ◽  
Vol 164 (6) ◽  
pp. 811-817 ◽  
Author(s):  
Carlo Iomini ◽  
Karla Tejada ◽  
Wenjun Mo ◽  
Heikki Vaananen ◽  
Gianni Piperno
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Primary Cilia ◽  
Umbilical Vein ◽  
Intraflagellar Transport ◽  
Mechanical Stimuli ◽  
Laminar Shear Stress ◽  
Human Endothelial Cells ◽  
Umbilical Vein Endothelial Cells ◽  
Laminar Shear

We identified primary cilia and centrosomes in cultured human umbilical vein endothelial cells (HUVEC) by antibodies to acetyl-α-tubulin and capillary morphogenesis gene-1 product (CMG-1), a human homologue of the intraflagellar transport (IFT) protein IFT-71 in Chlamydomonas. CMG-1 was present in particles along primary cilia of HUVEC at interphase and around the oldest basal body/centriole at interphase and mitosis. To study the response of primary cilia and centrosomes to mechanical stimuli, we exposed cultured HUVEC to laminar shear stress (LSS). Under LSS, all primary cilia disassembled, and centrosomes were deprived of CMG-1. We conclude that the exposure to LSS ends the IFT in cultured endothelial cells.

Laminar shear stress promotes mitochondrial homeostasis in endothelial cells

2018 ◽  
Vol 233 (6) ◽  
pp. 5058-5069 ◽  
Author(s):  
Li-Hong Wu ◽  
Hao-Chun Chang ◽  
Pei-Ching Ting ◽  
Danny L. Wang
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Laminar Shear Stress ◽  
Mitochondrial Homeostasis ◽  
Laminar Shear

A Promoter Polymorphism Regulates NFKB1 Gene Transactivity in Human Endothelial Cells under Laminar Shear Stress

2006 ◽  
Vol 38 (Supplement) ◽  
pp. S4
Author(s):  
Joon Y. Park ◽  
Iain K. Farrance ◽  
Hanjoong Jo ◽  
Steven R. Brant ◽  
Stephen M. Roth ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Promoter Polymorphism ◽  
Laminar Shear Stress ◽  
Human Endothelial Cells ◽  
Laminar Shear

AXL ACTIVATION MEDIATES LAMINAR SHEAR STRESS ANTIAPOPTOTIC EFFECTS IN HUMAN ENDOTHELIAL CELLS

2004 ◽  
Vol 13 (3) ◽  
pp. 194
Author(s):  
Daniela D'Arcangelo ◽  
Valeria Ambrosino ◽  
Gianluca Ragone ◽  
Maria Giannuzzo ◽  
Maurizio C Capogrossi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Laminar Shear Stress ◽  
Human Endothelial Cells ◽  
Laminar Shear

Laminar shear stress inhibits CXCR4 expression on endothelial cells: functional consequences for atherogenesis

2005 ◽  
Vol 19 (6) ◽  
pp. 1-25 ◽  
Author(s):  
Roberta Melchionna ◽  
Daniele Porcelli ◽  
Antonella Mangoni ◽  
Daniele Carlini ◽  
Giovanna Liuzzo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Cxcr4 Expression ◽  
Laminar Shear Stress ◽  
Functional Consequences ◽  
Laminar Shear

Laminar Shear Stress Promotes Nicotine-Induced Inflammation and Hemostatic Expression in Human Endothelial Cells

2016 ◽  
Vol 9 (3) ◽  
pp. 466-477 ◽  
Author(s):  
Yu-Hsiang Lee ◽  
Chi-Chung Lee ◽  
Chien-Hsun Huang ◽  
Feng-Ming Ho
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Laminar Shear Stress ◽  
Human Endothelial Cells ◽  
Laminar Shear

Recruitment of endothelial caveolae into mechanotransduction pathways by flow conditioning in vitro

2003 ◽  
Vol 285 (4) ◽  
pp. H1720-H1729 ◽  
Author(s):  
Victor Rizzo ◽  
Christine Morton ◽  
Natacha DePaola ◽  
Jan E. Schnitzer ◽  
Peter F. Davies
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Cell Surface ◽  
Tyrosine Phosphorylation ◽  
Surface Proteins ◽  
Luminal Surface ◽  
Laminar Shear Stress ◽  
Caveolin 1 ◽  
Cultured Endothelial Cells ◽  
Laminar Shear

The luminal surface of rat lung microvascular endothelial cells in situ is sensitive to changing hemodynamic parameters. Acute mechanosignaling events initiated in response to flow changes in perfused lung microvessels are localized within specialized invaginated microdomains called caveolae. Here we report that chronic exposure to shear stress alters caveolin expression and distribution, increases caveolae density, and leads to enhanced mechanosensitivity to subsequent changes in hemodynamic forces within cultured endothelial cells. Flow-preconditioned cells expressed a fivefold increase in caveolin (and other caveolar-residing proteins) at the luminal surface compared with no-flow controls. The density of morphologically identifiable caveolae was enhanced sixfold at the luminal cell surface of flow-conditioned cells. Laminar shear stress applied to static endothelial cultures (flow step of 5 dyn/cm2), enhanced the tyrosine phosphorylation of luminal surface proteins by 1.7-fold, including caveolin-1 by 1.3-fold, increased Ser1179 phosphorylation of endothelial nitric oxide synthase (eNOS) by 2.6-fold, and induced a 1.4-fold activation of mitogen-activated protein kinases (ERK1/2) over no-flow controls. The same shear step applied to endothelial cells preconditioned under 10 dyn/cm2 of laminar shear stress for 6 h and induced a sevenfold increase of total phosphotyrosine signal at the luminal endothelial cell surface enhanced caveolin-1 tyrosine phosphorylation 5.8-fold and eNOS phosphorylation by 3.3-fold over static control values. In addition, phosphorylated caveolin-1 and eNOS proteins were preferentially localized to caveolar microdomains. In contrast, ERK1/2 activation was not detected in conditioned cells after acute shear challenge. These data suggest that cultured endothelial cells respond to a sustained flow environment by directing caveolae to the cell surface where they serve to mediate, at least in part, mechanotransduction responses.

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