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Biological research · Mar 2021
LncRNA MALAT1 aggravates oxygen-glucose deprivation/reoxygenation-induced neuronal endoplasmic reticulum stress and apoptosis via the miR-195a-5p/HMGA1 axis.
- Ying Jia, Lian Yi, Qianqian Li, Tingjiao Liu, and Shanshan Yang.
- Department of Neurology, The First Affiliated Hospital of Harbin Medical University, No.23 Youzheng Street, Nangang District, Harbin, 150081, Heilongjiang, People's Republic of China.
- Biol. Res. 2021 Mar 9; 54 (1): 8.
BackgroundThis study aimed to investigate the potential role and molecular mechanism of lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in cerebral ischemia/reperfusion injury.ResultsUsing an oxygen-glucose deprivation/reoxygenation (OGD/R) cell model, we determined that the expression of MALAT1 was significantly increased during OGD/R. MALAT1 knockdown reversed OGD/R-induced apoptosis and ER stress. Mechanistically, MALAT1 promoted OGD/R-induced neuronal injury through sponging miR-195a-5p to upregulating high mobility group AT-hook1 (HMGA1).ConclusionsCollectively, these data demonstrate the mechanism underlying the invovlvement of MALAT1 in cerebral ischemia/reperfusion injury, thus providing translational evidence that MALAT1 may serve as a novel biomarker and therapeutic target for ischemic stroke.
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