Abstract
MicroRNA-126 (miR-126) is an endothelial-specific microRNA that has shown beneficial effects on endothelial dysfunction. However, the underlying molecular mechanism is unclear. The present study evaluated the effects of miR-126 on the cell migration and underlying mechanism in HUVECs treated with palmitate. The present results demonstrated that overexpression of miR-126 was found to decrease cell migration in palmitate-treated HUVECs, with decreased MLCK expression and subsequent decreased phosphorylated MLC level. miR-126 also decreased the phosphorylation of MYPT1 in palmitate-treated HUVECs. In addition, it was demonstrated that miR-126 decreases expression of the NADPH oxidase subunits, p67 and Rac family small GTPase 1 with a subsequent decrease in cell apoptosis. Moreover, the phosphorylation of ERK was reduced by miR-126 in palmitate-induced HUVECs. Taken together, the present study showed that the effect of miR-126 on cell migration and cell apoptosis is mediated through downregulation of MLCK via the ERK/MAPK pathway.
Highlights
Atherosclerosis (AS) is a chronic progressive pathological process characterized by multiple factors
The present results demonstrated that the expression of myosin regulatory light chain (MLC) in palmitatetreated human umbilical vein endothelial cells (HUVECs) was not significantly different compared with oleate-treated HUVECs, the phosphorylated MLC/MLC ratio in palmitate-treated HUVECs was increased compared with oleate-treated HUVECs, andmiR-126 mimic significantly decreased MLC phosphorylation (Figures 2B,D)
These results indicated that miR-126 reduced the phosphorylation of MLC by regulate the expression of Myosin light chain kinase (MLCK) and the phosphorylation of MYPT1 in palmitate-treated HUVECs
Summary
Atherosclerosis (AS) is a chronic progressive pathological process characterized by multiple factors. Endothelial dysfunction is the earliest step in the pathogenesis of AS (Gimbrone and García-Cardeña, 2016). A main component of saturated fat, is associated with increased cardiovascular disease risk. Clinical and experimental studies have demonstrated that high concentrations of free fatty acid (FFA) in the plasma, promotes endothelial dysfunction (Arijit et al, 2017). Palmitate increased monocyte expression of CD11b, which was associated with increased adhesion to rat aortic endothelium and CD36 expression, which promoted oxidized LDL uptake (Gao et al, 2012).
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