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Unraveling the mechanisms involved in endothelial barrier protective effects of angiopoietin-1 variant MAT.Ang-1

Ru-Yuan Zhang, Dong Min, Jun Wu, Lei Li, Hong-Ping Qu and Yao-Qing Tang*

Author Affiliations

Department of Critical Care Medicine, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China

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Critical Care 2012, 16:466  doi:10.1186/cc11844

See related research by Alfieri et al.,

Published: 27 November 2012

First paragraph (this article has no abstract)

With great interest we read the recent article by Alfieri and colleagues [1], demonstrating that angiopoietin (Ang)-1 variant MAT.Ang-1 improved endotoxemiainduced microvascular dysfunction and microvascular hyperpermeability. The authors suggested that MAT. Ang-1-induced recovery of microcirculatory tissue perfusion during sepsis is due to preservation of endothelial barrier integrity. To further elucidate the mechanism, they investigated the possibility of involvement of VE-cadherin, a major adherens junctions protein responsible for microvascular leakage in inflammation. They found, however, while there was no change in overall expression of VE-cadherin, MAT.Ang-1 increased VE-cadherin phosphorylation in the treated mice, which appears unable to explain the observed endothelial barrier protective effects of MAT.Ang-1.