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

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.

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

Cardiovascular Pathology ◽

10.1016/j.carpath.2004.03.585 ◽

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

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

Cellular and Molecular Bioengineering ◽

10.1007/s12195-016-0434-y ◽

2016 ◽

Vol 9 (3) ◽

pp. 466-477 ◽

Cited By ~ 2

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

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Axl receptor activation mediates laminar shear stress anti-apoptotic effects in human endothelial cells

Cardiovascular Research ◽

10.1016/j.cardiores.2006.06.002 ◽

2006 ◽

Vol 71 (4) ◽

pp. 754-763 ◽

Cited By ~ 30

Author(s):

D DARCANGELO ◽

V AMBROSINO ◽

M GIANNUZZO ◽

C GAETANO ◽

M CAPOGROSSI

Keyword(s):

Endothelial Cells ◽

Shear Stress ◽

Receptor Activation ◽

Laminar Shear Stress ◽

Human Endothelial Cells ◽

Apoptotic Effects ◽

Laminar Shear

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Endothelin receptor B-mediated induction of c-jun and AP-1 in response to shear stress in human endothelial cellsThis article is one of a selection of papers published in the special issue (part 2 of 2) on Forefronts in Endothelin.

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y08-026 ◽

2008 ◽

Vol 86 (8) ◽

pp. 499-504 ◽

Cited By ~ 2

Author(s):

H. Morawietz ◽

A.H. Wagner ◽

M. Hecker ◽

W. Goettsch

Keyword(s):

Endothelial Cells ◽

Shear Stress ◽

Endothelin Receptor ◽

Laminar Shear Stress ◽

Human Endothelial Cells ◽

Endothelin 1 ◽

Subtype B ◽

Short Term Exposure ◽

Stress Dependent ◽

Laminar Shear

In vivo, endothelial cells are constantly exposed to shear stress by flowing blood. Short-term exposure of endothelial cells to shear stress has been shown to induce endothelin-1 release. It is currently unknown, however, whether this shear stress-dependent endothelin-1 release affects the expression and activity of transcription factors. In this study, primary cultures of human endothelial cells from the umbilical vein were exposed to laminar shear stress in a cone-and-plate viscometer. Laminar shear stress for 30 min induced a 2-fold increase in mRNA expression of c-jun , but not c-fos, in human endothelial cells. Blockade of endothelin receptor subtype B (ETB) with BQ788 prevented this shear stress-dependent induction of c-jun expression. The induction of c-jun by shear stress involved protein kinase C and endothelial NO synthase. In addition, exposure of endothelial cells to arterial laminar shear stress for 1 h increased the binding of transcription factor AP-1 to its consensus sequence by 1.7-fold in electrophoretic mobility shift assays. This induction was also mediated by an ETB-dependent pathway. Supershift analysis supports an AP-1 complex containing c-jun, but not c-fos, in human endothelial cells. In conclusion, our data suggest endothelin-1-mediated induction of c-jun expression and activation of AP-1 (possibly as a c-jun homodimer) by laminar shear stress in human endothelial cells.

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