High Fluid Shear Stress Inhibits Cytokine-Driven Smad2/3 Activation in Vascular Endothelial Cells.

ABSTRACT: Background Atherosclerosis occurs preferentially in regions of low and disturbed fluid shear stress (FSS) but is limited in regions of high laminar FSS as a result of inhibition of endothelial inflammatory pathways. Recent work has identified endothelial to mesenchymal transition (EndMT) driven by TGFβ2 (transforming growth factor beta 2)-Smad2/3 (mothers against decapentaplegic) signaling as a critical component of atherogenesis. However, interactions between FSS and EndMT in this context have not been investigated. Methods and Results Endothelial cells were treated with TGFβ2 and inflammatory cytokines (interleukin 1β and tumor necrosis factor alpha) with or without high FSS in a parallel plate flow chamber. Smad2/3 nuclear translocation and target gene expression, assayed by immunofluor

SUBMITTER: Deng H 

PROVIDER: S-EPMC9707828 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature