LncRNA MALAT1 aggravates oxygen-glucose deprivation/reoxygenation-induced
neuronal endoplasmic reticulum stress and apoptosis via the miR-195a-5p/HMGA1
axis.
Jia Y(1), Yi L(1), Li Q(1), Liu T(1), Yang S(2). Author information:
(1)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.
(2)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. [Email]
BACKGROUND: This study aimed to investigate the potential role and molecular mechanism of lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in cerebral ischemia/reperfusion injury. RESULTS: Using 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). CONCLUSIONS: Collectively, 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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