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. 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). 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.

中文翻译：

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LncRNA MALAT1 通过 miR-195a-5p/HMGA1 轴加重氧-葡萄糖剥夺/复氧诱导的神经元内质网应激和细胞凋亡

本研究旨在探讨lncRNA转移相关肺腺癌转录物1（MALAT1）在脑缺血/再灌注损伤中的潜在作用和分子机制。使用氧-葡萄糖剥夺/复氧 (OGD/R) 细胞模型，我们确定 MALAT1 的表达在 OGD/R 期间显着增加。MALAT1 敲低逆转 OGD/R 诱导的细胞凋亡和 ER 应激。从机制上讲，MALAT1 通过将 miR-195a-5p 上调高迁移率组 AT-hook1 (HMGA1) 促进 OGD/R 诱导的神经元损伤。总的来说，这些数据证明了 MALAT1 参与脑缺血/再灌注损伤的机制，从而提供了 MALAT1 可作为缺血性中风的新型生物标志物和治疗靶点的转化证据。