Cardiology Medical News about Phosphorylation

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Phosphorylation of Caveolin-1 Regulates Oxidant–Induced Pulmonary Vascular Permeability via Paracellular and Transcellular Pathways
Circulation Research, 08/31/09

Sun Y et al. – Caveolin–1 phosphorylation–dependent signaling plays a crucial role in oxidative stress–induced pulmonary vascular hyperpermeability via transcellular and paracellular pathways. Thus, caveolin–1 phosphorylation may be an important therapeutic target for limiting oxidant–mediated vascular hyperpermeability, protein–rich edema formation, and acute lung injury.

Exclusive Author Commentary
Guochang Hu, 08/31/09

This study provides strong evidence indicating that caveolin-1 phosphorylation in endothelial cells plays a fundamental role in the mechanism of oxidant-induced pulmonary vascular hyperpermeability. Oxidant-induced increase in caveolae-mediated albumin transport and decrease in endothelial barrier integrity were both dependent on tyrosine phosphorylation of caveolin-1, suggesting caveolin-1 phosphorylation is a common signal regulating transcellular and paracellular permeability pathways in lung microvessels. Although these studies focused on oxidative stress as a means of increasing endothelial permeability and inducing acute lung injury, it is possible that our findings have broader applicability in understanding the mechanisms and development of inflammatory pulmonary vascular hyperpermeability. Therefore, therapeutic inhibition of caveolin-1 phosphorylation may be an effective means of limiting lung vascular injury by preventing increased transcellular albumin permeability and stabilizing the endothelial junctional barrier.

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