MicroRNA-142-3p modulates atherosclerosis-associated endothelial cell apoptosis via targeting Rictor |
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Authors: | XIAO Li LIU Ping QIN Bing |
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Institution: | Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China |
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Abstract: | AIM To investigate the role of microRNA-142-3p (miR-142-3p) in endothelial cell apoptosis during atherosclerosis (AS) and the underlying mechanism. METHODS Human aortic endothelial cells (HAECs) were treated with oxidized low-density lipoprotein (ox-LDL). The expression level of miR-142-3p was detected by RT-qPCR. Apoptosis was determined via flow cytometry (FCM) and caspase-3 activity assay. Prediction of the binding site between miR-142-3p and 3’-UTR of Rictor mRNA was performed by bioinformatics analysis and confirmed by dual-luciferase reporter assay. RESULTS The expression of miR-142-3p was substantially up-regulated during the ox-LDL-elicited apoptosis in HAECs (P<0.05,P<0.01). Forced expression of miR-142-3p exacerbated apoptosis in HAECs whereas inhibition of miR-142-3p partly alleviated apoptotic cell death mediated by ox-LDL. Further analysis identified Rictor as a direct target gene of miR-142-3p, and Rictor knock-down abolished the anti-apoptotic effect of miR-142-3p inhibitor. Moreover, the Akt/endothelial nitric oxide synthase (eNOS) signaling pathway was found to mediate the beneficial effect of miR-142-3p inhibitor on endothelial cells apoptosis. CONCLUSION Down-regulation of miR-142-3p inhibits endothelial cell apoptosis and atherosclerotic development by up-regulating the expression of Rictor and activating the Akt/eNOS signaling pathway. |
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Keywords: | MicroRNA-142-3p Human aortic endothelial cells Apoptosis Rictor Atherosclerosis |
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