Jiangping Cai1, Shina Shangguan2, Guoqian Li1, Yazhen Cai1, Yuanjie Chen1, Gaoting Ma3,4,5, Zhongrong Miao3,4,5, Lian Liu3,4,5, Yiming Deng3,4,5. 1. Department of Neurology, The First Hospital of Quanzhou Affiliated to Fujian Medical University , Quanzhou , People's Republic of China. 2. Department of Neurology, Shandong University/Affiliated Hospital of Shandong Medical College , Jinan City , China. 3. Departments of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University , Beijing , China. 4. China National Clinical Research Center for Neurological Diseases , Beijing , China. 5. Center of Stroke, Beijing Institute for Brain Disorders , Beijing , China.
Abstract
Aims: In previous studies, numerous differential lncRNAs in cerebral ischemic reperfusion injury were identified using RNA-Seq analysis. However, little is known about whether and how lncRNAs involved in cerebral I/R injury. In this study, we investigated the function and explored the possible mechanism of lncRNA Gm11974 in cerebral I/R injury. Methods: Oxygen glucose deprivation model in N2a cells were utilized to mimic the cerebral I/R injury in vitro. Trypan blue staining, Tunel, JC-1 and cell viability were measured to evaluate the function of lncRNA Gm11974. Dual-luciferase reporter assay was used to explore the potential mechanism of lncRNA Gm11974. Results: Gm11974 was mainly located in cytoplasm. Knockdown of lncRNA Gm11974 alleviated the apoptosis induced by OGD and cell death rates were significantly reduced. We further provided the possible mechanism that Gm11974/miR-766-3p/NR3C2 axis plays important role in cerebral I/R injury. Conclusions: We evaluated the function and mechanism of lncRNA Gm11974 in ischemic brain injury. LncRNA Gm11974 may serve as a potential target for new therapeutic intervention.
Aims: In previous studies, numerous differential lncRNAs in cerebral ischemic reperfusion injury were identified using RNA-Seq analysis. However, little is known about whether and how lncRNAs involved in cerebral I/R injury. In this study, we investigated the function and explored the possible mechanism of lncRNA Gm11974 in cerebral I/R injury. Methods:Oxygenglucose deprivation model in N2a cells were utilized to mimic the cerebral I/R injury in vitro. Trypan blue staining, Tunel, JC-1 and cell viability were measured to evaluate the function of lncRNA Gm11974. Dual-luciferase reporter assay was used to explore the potential mechanism of lncRNA Gm11974. Results:Gm11974 was mainly located in cytoplasm. Knockdown of lncRNA Gm11974 alleviated the apoptosis induced by OGD and cell death rates were significantly reduced. We further provided the possible mechanism that Gm11974/miR-766-3p/NR3C2 axis plays important role in cerebral I/R injury. Conclusions: We evaluated the function and mechanism of lncRNA Gm11974 in ischemic brain injury. LncRNA Gm11974 may serve as a potential target for new therapeutic intervention.
Authors: Yanqun Cao; Jia Liu; Quzhe Lu; Kai Huang; Baolin Yang; James Reilly; Na Jiang; Xinhua Shu; Lei Shang Journal: Int J Mol Med Date: 2022-05-20 Impact factor: 5.314