Endothelial mechanisms for inactivation of inflammation-induced hyperpermeability

作者：Prerna R. Nepali, Pía C. Burboa, Mauricio A. Lillo, Patricio E. Mujica, Toru Iwahashi, Jihang Zhang, Ricardo G. Durán, Mauricio P. Borić, Nikola Golenhofen, David D. Kim, Natascha G. Alves, Andrew P. Thomas, Jerome W. Breslin, Fabiola A. Sánchez, Walter N. Durán · 发表于：American Journal of Physiology-Heart and Circulatory Physiology · 年份：2023 · DOI：10.1152/ajpheart.00543.2022 · 被引用次数：12 · 研究领域：Blood Coagulation and Thrombosis Mechanisms、Adipokines, Inflammation, and Metabolic Diseases、Nitric Oxide and Endothelin Effects

Termination of microvascular hyperpermeability has been so far accepted to be a passive result of the removal of the applied proinflammatory agonists. We provide in vivo and in vitro evidence that 1) inactivation of hyperpermeability is an actively regulated process, 2) proinflammatory agonists (PAF and VEGF) stimulate microvascular hyperpermeability and initiate endothelial mechanisms that terminate hyperpermeability, and 3) eNOS location-translocation is critical in the activation-inactivation cascade of endothelial hyperpermeability.