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- W3157691808 abstract "Acute respiratory distress syndrome (ARDS) is a severe yet predictable complication of covid-19, the novel coronavirus disease 2019, caused by severe acute respiratory syndrome coronavirus-2 (sars-cov-2). Comprehensive understanding of the pathogenesis of COVID-19-induced ARDS at the cellular and molecular levels is important for developing effective early preventive and therapeutic interventions. Sars-cov-2 utilizes angiotensin-converting enzyme 2 (ACE2) on the surface of the host cell to gain its entry and, in the meantime, suppresses ACE2 expression and function. The decrease in available ACE2 results in excessive production of angiotensin II (Ang II), a potent Gq-linked agonist that can increase cytosolic Ca2+ concentration causing lung vascular endothelial cell barrier disruption, an essential early step in the pathogenesis of ARDS, ultimately leading to pulmonary edema and subsequent respiratory compromise. In the present study, we first established that pulmonary microvascular endothelial cells (PMVECs) possess a Ca2+/MLC2 (regulatory myosin light chain 2) signaling pathway that controls endothelial cell barrier function. Ionomycin, a potent Ca2+-selective ionophore, induced a rapid inter-EC gap formation along with a rapid, dose-dependent MLC2 phosphorylation in PMVECs. Chelation of extracellular Ca2+ or direct inhibition of MLC2 phosphorylation abolished the ionomycin-induced inter-EC gap formation. Next, we demonstrated that Ang II also induced inter-EC gap formation and a dose-dependent increase in MLC2 phosphorylation in PMVECs. Thus, Ang II may activate the Ca2+/MLC2 signaling pathway to disrupt lung microvascular endothelial barrier. These findings suggest a potential causative link between sars-cov-2 infection, Ca2+-dependent regulatory myosin light chain activation, and lung vascular endothelial barrier disruption in COVID-19-induced ARDS." @default.
- W3157691808 created "2021-05-10" @default.
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- W3157691808 date "2021-05-01" @default.
- W3157691808 modified "2023-09-25" @default.
- W3157691808 title "Angiotensin II Potentiation Contributes to Inter-Endothelial Cell Gap Formation in Pulmonary Microvascular Endothelial Cells Through Regulatory Myosin Light Chain 2 Phosphorylation" @default.
- W3157691808 doi "https://doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4386" @default.
- W3157691808 hasPublicationYear "2021" @default.
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