Endothelial cell Piezo1 mediates pressure-induced lung vascular hyperpermeability via disruption of adherens junctions Article Swipe

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Adherens junction PIEZO1 Pulmonary edema Hydrostatic pressure Lung Endothelial stem cell Edema Vascular permeability Endothelium Medicine Tight junction VE-cadherin Cell biology Pathology Chemistry Biology Cell Cadherin Internal medicine Biochemistry Mechanosensitive channels Ion channel Physics Thermodynamics Receptor In vitro

Emily E. Friedrich , Zhigang Hong , Shiqin Xiong , Ming Zhong , Anke Di , Jalees Rehman , Yulia Komarova , Asrar B. Malik ·

YOU? · · 2019 · Open Access · · DOI: https://doi.org/10.1073/pnas.1902165116 · OA: W2951672374

Significance Increased hydrostatic pressure in lung capillaries experienced during high altitude, head trauma, and left heart failure can lead to disruption of lung endothelial barrier and edema formation. We identified Piezo1 as a mechanical sensor responsible for endothelial barrier breakdown (barotrauma) secondary to reduced expression of the endothelial adherens junction proteins VE-cadherin, β-catenin, and p120-catenin. Endothelial-specific deletion or pharmacological inhibition of Piezo1 prevented lung capillary leakage, suggesting a therapeutic approach for preventing edema and associated lung failure.