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.

Effects of Laminar Shear Stress on Mitochondrial Biogenesis in Human Umbilical Vein Endothelial Cells

2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 464
Author(s):  
BOA KIM ◽  
Ji-Seok Kim ◽  
Deborah L. Feairheller ◽  
Kathleen M. Sturgeon ◽  
Michael D. Brown ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Mitochondrial Biogenesis ◽  
Umbilical Vein ◽  
Laminar Shear Stress ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
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

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.

2008 ◽  
Vol 86 (8) ◽  
pp. 499-504 ◽  
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.

Flow-induced expression of endothelial Na-K-Cl cotransport: dependence on K+ and Cl− channels

2001 ◽  
Vol 280 (1) ◽  
pp. C216-C227 ◽  
Author(s):  
Jimmy Suvatne ◽  
Abdul I. Barakat ◽  
Martha E. O'Donnell
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Umbilical Vein ◽  
Fold Increase ◽  
Flow Chamber ◽  
Steady Shear ◽  
Laminar Shear Stress ◽  
Protein Levels ◽  
Steady Laminar Shear Stress ◽  
Umbilical Vein Endothelial Cells

Steady laminar shear stress has been shown previously to markedly increase Na-K-Cl cotransporter mRNA and protein in human umbilical vein endothelial cells and also to rapidly increase endothelial K+ and Cl− channel conductances. The present study was done to evaluate the effects of shear stress on Na-K-Cl cotransporter activity and protein expression in bovine aortic endothelial cells (BAEC) and to determine whether changes in cotransporter expression may be dependent on early changes in K+ and Cl− channel conductances. Confluent BAEC monolayers were exposed in a parallel-plate flow chamber to either steady shear stress (19 dyn/cm2) or purely oscillatory shear stress (0 ± 19 dyn/cm2) for 6–48 h. After shearing, BAEC monolayers were assessed for Na-K-Cl cotransporter activity or were subjected to Western blot analysis of cotransporter protein. Steady shear stress led to a 2- to 4-fold increase in BAEC cotransporter protein levels and a 1.5- to 1.8-fold increase in cotransporter activity, increases that were sustained over the longest time periods studied. Oscillatory flow, in contrast, had no effect on cotransporter protein levels. In the presence of flow-sensitive K+ and Cl− channel pharmacological blockers, the steady shear stress-induced increase in cotransporter protein was virtually abolished. These results suggest that shear stress modulates the expression of the BAEC Na-K-Cl cotransporter by mechanisms that are dependent on flow-activated ion channels.

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