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. 2021 Apr 1;22(7):3684. doi: 10.3390/ijms22073684

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Regulation of vascular permeability by Rho GTPases. In ECs, vascular endothelial growth factor (VEGF) A and tumor necrosis factor (TNF) α activate Rac1 via Vav2 and P-Rex1, respectively, leading to the PAK-mediated phosphorylation, internalization and degradation of VE-cadherin. The RhoA-mediated contraction of radial actin bundles further destabilizes VE-cadherin-based EC–EC junctions and neural (N)-cadherin-based EC-pericyte junctions. Angiopoietin-1 (Ang1) prevents VEGF-A-induced VE-cadherin degradation via the RhoA-mDia1-mediated inhibition of Rac1 activation. In addition, Ang1 suppresses actomyosin contraction at the EC–EC junctions by inactivating RhoA via Rac1 and p190 RhoGAP. The Rac1-mediated recruitment of N-cadherin also protects EC-pericyte junctions.