Article
RhoA S-nitrosylation as a regulatory mechanism influencing endothelial barrier function in response to G+-bacterial toxins.
Biochemical pharmacology - 1 Mar 2017
Chen F, Wang Y, Rafikov R, Haigh S, Zhi W B, Kumar S, Doulias P T, Rafikova O, Pillich H, Chakraborty T, Lucas R, Verin A D, Catravas J D, She J X, Black S M, Fulton D J R
Abstract excerpt
Disruption of the endothelial barrier in response to Gram positive (G+) bacterial toxins is a major complication of acute lung injury (ALI) and can be further aggravated by antibiotics which stimulate toxin release. The integrity of the pulmonary endothelial barrier is mediated by the balance of disruptive forces such as the small GTPase RhoA, and protective forces including endothelium-derived nitric oxide (NO)....
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