Depletion of Arg/Abl2 improves endothelial cell adhesion and prevents vascular leak during inflammation.

ABSTRACT: Endothelial barrier disruption and vascular leak importantly contribute to organ dysfunction and mortality during inflammatory conditions like sepsis and acute respiratory distress syndrome. We identified the kinase Arg/Abl2 as a mediator of endothelial barrier disruption, but the role of Arg in endothelial monolayer regulation and its relevance in vivo remain poorly understood. Here we show that depletion of Arg in endothelial cells results in the activation of both RhoA and Rac1, increased cell spreading and elongation, redistribution of integrin-dependent cell-matrix adhesions to the cell periphery, and improved adhesion to the extracellular matrix. We further show that Arg is activated in the endothelium during inflammation, both in murine lungs exposed to barrier-disruptive agents, an

SUBMITTER: Amado-Azevedo J 

PROVIDER: S-EPMC7996118 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature