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Cyclic pressure modulates endothelial barrier function.

H Y Shin1, R Bizios, M E Gerritsen

  • 1Department of Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, New York, USA.

Endothelium : Journal of Endothelial Cell Research
|September 18, 2003
PubMed
Summary
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Physiological cyclic pressure selectively impacts endothelial barrier function. Higher pressures alter tight junction protein distribution (zona occludens-1) and F-actin cytoskeleton, affecting permeability to albumin.

Area of Science:

  • Physiology
  • Cell Biology
  • Biomechanics

Background:

  • Mechanical forces significantly influence endothelial cell functions.
  • Endothelial barrier function regulation by physical stimuli remains incompletely understood.

Purpose of the Study:

  • To investigate the effects of physiologically relevant cyclic pressures on human umbilical vein endothelial cell (HUVEC) barrier function.
  • To elucidate the molecular mechanisms underlying pressure-induced changes in endothelial barrier integrity.

Main Methods:

  • HUVECs were exposed to sinusoidal cyclic pressures using a custom-designed system.
  • Transendothelial permeability to albumin was measured.
  • Immunofluorescence microscopy was used to assess the localization of tight junction protein zona occludens-1 (ZO-1) and adherens junction proteins (VE-cadherin, beta-catenin), as well as F-actin cytoskeleton reorientation.

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Main Results:

  • Cyclic pressure of 140/100 mm Hg, but not 60/20 mm Hg, at 1 Hz for 18 hours significantly reduced transendothelial permeability to albumin.
  • These pressure-induced changes in barrier function correlated with the redistribution of intracellular zona occludens-1 (ZO-1).
  • F-actin cytoskeleton reorientation was observed, while adherens junction proteins (VE-cadherin, beta-catenin) localization remained unaffected.

Conclusions:

  • Specific levels of cyclic pressure, relevant to the vascular hemodynamic environment, modulate endothelial barrier function.
  • Altered distribution of the tight junction component ZO-1 is associated with these pressure-induced changes in endothelial barrier function.