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        LncRNA MALAT1 protects human umbilical vein endothelial cells against ox-LDL triggered cell death through regulation of MGP

        Xia Wang,Hongqin Zhao,Shaonan Yang,Xiaojun Shao,Shumin Nie,Xudong Pan 대한독성 유전단백체 학회 2019 Molecular & cellular toxicology Vol.15 No.3

        Backgrounds: Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is an lncRNA that has been suggested as a key regulator in the onset of atherosclerosis (AS). This study described the role of MALAT1 in oxidized low density lipoprotein (ox-LDL)-induced endothelial cells death. Methods: Human umbilical vein endothelial cells (HUVECs) were subjected to ox-LDL, before which the expression of MALAT1 was overexpressed by transfection. CCK-8 assay, flow cytometer detection, and western blot were carried out to evaluate cell viability, apoptosis and autophagy. qRT-PCR and western blot analyses were performed to investigate the regulatory relationship between MALAT1, Matrix Gla protein (MGP) and mTOR signaling to decode the underlying mechanism. Results: Up-regulation of MALAT1 attenuated ox-LDLinduced HUVECs lose, as evidenced by the promoted cell viability, and the decreased apoptosis rate. This finding was coupled with the down-regulated p53, Bax, active-caspase-3, Beclin-1 and LC3-II, as well as the up-regulated Bcl-2 and p62. Meanwhile, MALAT1 upregulation promoted the phosphorylation of p70S6K and mTOR, and the expression of MGP. MGP up-regulation exhibited MALAT1-like propoties in preventing ox-LDL-induced cell death and mTOR deactivation. Of contrast, MGP silence affected HUVECs survival and mTOR signaling resulted in contrary impacts. Conclusion: The present work described that MALAT1 up-regulation prevented ox-LDL-mediated apoptosis and autophagy in HUVECs. The protective effects of MALAT1 might be partially via up-regulating MGP, which led to the activation of mTOR signaling.

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