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Related Concept Videos

Shearing Stress01:18

Shearing Stress

Shearing stress, denoted by the Greek letter tau (τ), is stress caused by forces acting transversely on an object. These forces create internal ones within the entity in the plane where the external forces are applied. The resultant of these internal forces is the shear in the section.
The average shearing stress can be calculated by dividing the shear by the area of the cross-section.
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...

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Related Experiment Video

Updated: May 12, 2026

The Assembly and Application of 'Shear Rings': A Novel Endothelial Model for Orbital, Unidirectional and Periodic Fluid Flow and Shear Stress
09:20

The Assembly and Application of 'Shear Rings': A Novel Endothelial Model for Orbital, Unidirectional and Periodic Fluid Flow and Shear Stress

Published on: October 31, 2016

Shear stress regulates endothelial microparticle release.

Anne-Clémence Vion1, Bhama Ramkhelawon, Xavier Loyer

  • 1INSERM, U970, Paris Cardiovascular Research Center PARCC, Paris, France.

Circulation Research
|March 29, 2013
PubMed
Summary
This summary is machine-generated.

Endothelial cells release microparticles (MPs) when exposed to low shear stress (SS) via Rho kinases and ERK1/2 pathways. High SS inhibits MP release through nitric oxide (NO)-dependent regulation of ABCA1 expression and cytoskeletal organization.

Keywords:
ABCA1endothelial cellsmicroparticlesnitric oxiderho kinaseshear stress

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Gene Expression Analysis of Endothelial Cells Exposed to Shear Stress Using Multiple Parallel-plate Flow Chambers

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Related Experiment Videos

Last Updated: May 12, 2026

The Assembly and Application of 'Shear Rings': A Novel Endothelial Model for Orbital, Unidirectional and Periodic Fluid Flow and Shear Stress
09:20

The Assembly and Application of 'Shear Rings': A Novel Endothelial Model for Orbital, Unidirectional and Periodic Fluid Flow and Shear Stress

Published on: October 31, 2016

Electrophysiological Recordings of Single-cell Ion Currents Under Well-defined Shear Stress
07:17

Electrophysiological Recordings of Single-cell Ion Currents Under Well-defined Shear Stress

Published on: August 2, 2019

Gene Expression Analysis of Endothelial Cells Exposed to Shear Stress Using Multiple Parallel-plate Flow Chambers
08:50

Gene Expression Analysis of Endothelial Cells Exposed to Shear Stress Using Multiple Parallel-plate Flow Chambers

Published on: October 21, 2018

Area of Science:

  • Cardiovascular Biology
  • Cellular Mechanotransduction
  • Endothelial Cell Biology

Background:

  • Endothelial activation and apoptosis release membrane-shed microparticles (EMPs), which are significant biological effectors.
  • Endothelial cells are crucial for vascular health, and their response to mechanical forces is key to understanding vascular disease.
  • Microparticles (MPs) are implicated in various physiological and pathological processes, including thrombosis and inflammation.

Purpose of the Study:

  • To investigate the hypothesis that laminar shear stress (SS) regulates endothelial microparticle (EMP) release.
  • To elucidate the signaling pathways and molecular mechanisms by which SS influences EMP release.
  • To determine the role of nitric oxide (NO) and ABCA1 expression in SS-mediated EMP release.

Main Methods:

  • Quantification of EMP levels in endothelial cells subjected to varying SS using flow cytometry.
  • Inhibition of specific signaling pathways, including extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and Rho kinases, and caspase pathways.
  • Assessment of endothelial Rho kinases and ERK1/2 activities, cytoskeletal reorganization, and RhoA activity.
  • Investigation of the effects of nitric oxide (NO) modulation using L-NG-nitroarginine methyl ester (L-NAME) and S-nitroso-N-acetyl-D,L-penicillamine (SNAP).
  • Analysis of ATP-binding cassette transporter A1 (ABCA1) expression under different SS conditions and NO modulation.

Main Results:

  • Low SS (2 dyne/cm(2)) significantly augmented EMP levels over time compared to high SS (20 dyne/cm(2)).
  • EMP release under low SS was sensitive to ERK1/2 and Rho kinases inhibitors, involving increased Rho kinases and ERK1/2 activities and cytoskeletal reorganization.
  • Overexpression of active RhoA stimulated EMP release even under high SS.
  • High SS-induced EMP release was increased by L-NAME (NO inhibition) and decreased by SNAP (NO donation), suggesting NO's inhibitory role.
  • ABCA1 expression was higher under low SS and modulated by NO, with L-NAME increasing it under high SS and SNAP decreasing it under low SS.

Conclusions:

  • Sustained atheroprone low SS stimulates EMP release via Rho kinases and ERK1/2 activation.
  • Atheroprotective high SS limits EMP release through NO-dependent regulation of ABCA1 expression and cytoskeletal organization.
  • Endothelial SS is identified as a critical physiological regulator of microparticle release, with implications for vascular health and disease.