TRPC6-dependent Ca2+ flux in endothelial cells after TLR4-induced diacylglycerol production mediates lung endothelial barrier disruption and inflammation induced by LPS.

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Background: Mechanisms linking cortical actin with adherens junctions (AJs) required for forming restrictive endothelial barrier remain unclear. Results: We show that neural Wiskott-Aldrich syndrome protein (N-WASP) binds AJ constituent, p120-catenin, forms cortical actin, and links AJs with actin. Conclusion: N-WASP stabilizes AJs and thereby maintains endothelial barrier function. Significance: N-WASP represents a novel target for preventing leaky endothelial barrier syndrome.

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