LncRNA MALAT1 aggravates oxygen‐glucose deprivation/reoxygenation-induced neuronal endoplasmic reticulum stress and apoptosis via the miR-195a-5p/HMGA1 axis

Biological research: BR

article

Jia, Ying¹  Yi, Lian¹  Li, Qianqian¹  Liu, Tingjiao¹  Yang, Shanshan¹ 

[1] Department of Neurology, The First Affiliated Hospital of Harbin Medical University

关键词: Ischemic stroke;    MALAT1;    Oxygen‐glucose deprivation/reoxygenation;    Neuronal injury;    Endoplasmic reticulum stress;   

DOI  :  10.1186/s40659-021-00331-9

来源: BioMed Central

【 摘 要 】

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.

【 授权许可】

Unknown