Simvastatin ameliorates oxygen glucose deprivation/reoxygenation-induced pulmonary endothelial barrier dysfunction by restoring cell-cell junctions and actin cytoskeleton dynamics via the PI3K/Akt signaling pathway.

Abstract:

:Endothelial barrier dysfunction is a critical pathophysiological process of pulmonary ischemia/reperfusion (I/R) injury in patients scheduled for cardiopulmonary bypass. Impaired actin cytoskeleton dynamics and cell-cell junctions are the main causes of endothelial dysfunction. Statins have protective effects on I/R-induced lung injury; however, the mechanism is unclear. We explored the therapeutic potential of simvastatin (SV) in endothelial cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R). SV pretreatment promoted the barrier function of human pulmonary microvascular endothelial cells (HPMECs) subjected to OGD/R. LY294002 was used to evaluate the role of the PI3K/Akt pathway in regulating the barrier function of HPMECs subjected to OGD/R. LY294002 suppressed the barrier function of HPMECs. SV restored the endothelial barrier function by rescuing endothelial cell migration and permeability, which are involved in the regulation of cytoskeleton dynamics and intercellular junction expression via the PI3K/Akt signaling pathway.

journal_name

Am J Transl Res

authors

Han D,Sun J,Fan D,Zhang C,Du S,Zhang W

subject

Has Abstract

pub_date

2020-09-15 00:00:00

pages

5586-5596

issue

9

issn

1943-8141

journal_volume

12

pub_type

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