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RhoA, RhoB and RhoC differentially regulate endothelial barrier function.

Manon C A Pronk1, Jan S M van Bezu1, Geerten P van Nieuw Amerongen1

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RhoB negatively regulates endothelial permeability in resting cells. RhoA and RhoB mediate thrombin-induced barrier dysfunction, while RhoC aids barrier repair.

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Area of Science:

  • Cell biology
  • Molecular biology
  • Physiology

Background:

  • Rho GTPases regulate actin dynamics and endothelial barrier function.
  • RhoA is well-studied, but RhoB and RhoC roles in endothelial barrier function are unclear.

Purpose of the Study:

  • To investigate the distinct or overlapping roles of RhoA, RhoB, and RhoC in endothelial barrier function and permeability.
  • To analyze their roles in both resting and activated endothelial cells.

Main Methods:

  • Primary endothelial cells were used.
  • siRNA transfection was employed for individual, double, or triple knockdown of RhoA, RhoB, and RhoC.
  • Endothelial permeability and VE-cadherin localization were assessed.

Main Results:

  • RhoB, not RhoA or RhoC, negatively regulates resting endothelial permeability.
  • Loss of RhoB led to VE-cadherin accumulation at cell-cell contacts.
  • Thrombin-induced endothelial barrier disruption involves RhoA and RhoB.
  • Combined RhoA/B knockdown reduced Myosin Light Chain phosphorylation and increased VE-cadherin at cell contacts post-thrombin.
  • RhoC supports Rac1-dependent endothelial barrier restoration.

Conclusions:

  • RhoA, RhoB, and RhoC differentially regulate endothelial barrier dynamics.
  • RhoB acts as a key regulator of basal endothelial permeability.
  • RhoA and RhoB are critical for thrombin-induced barrier dysfunction, whereas RhoC plays a role in barrier recovery.