Abstract
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.
Highlights
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
Long noncoding RNAs (LncRNAs) MALAT1 was upregulated in oxygen-glucose deprivation/reoxygenation (OGD/R)‐induced neuronal injury of HT22 cells The cell model of OGD/R-neuronal injury was established by 4 h OGD followed by 12 h, 24 h and 48 h reoxygenation in HT22 neural cells
The cell model of OGD/R-neuronal injury established by 4 h OGD followed by 48 h reoxygenation was chose for further experiments
Summary
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. Stroke is a common cerebrovascular disease and the third leading cause of death in China, with 1.57 million deaths in 2018 [1]. Ischemic stroke is by far the most common type of stroke, accounting for about 87 % of all strokes [2]. Thrombolysis therapy is the most effective strategy to restore cerebral blood flow timely for ischemic stroke patients [3]. Blood flow restoration improves the oxygen supply and induces the overproduction of ROS, activates inflammation and immune response, and triggers cell death programs [4]. A comprehensive understanding of the Endoplasmic reticulum (ER) stress pathway is an important apoptotic pathway and has been reported to induce apoptosis in numerous diseases including metabolic, neurodegenerative and cardiovascular diseases, cancer, inflammation, and viral infections [5].
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