Unraveling the mechanisms involved in endothelial barrier protective effects of angiopoietin-1 variant MAT.Ang-1
Department of Critical Care Medicine, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
Critical Care 2012, 16:466 doi:10.1186/cc11844
See related research by Alfieri et al., http://ccforum.com/content/16/5/R182
Published: 27 November 2012First 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.
