LncRNA SNHG3 promotes autophagy-induced neuronal cell apoptosis by acting as a ceRNA for miR-485 to up-regulate ATG7 exp
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ORIGINAL ARTICLE
LncRNA SNHG3 promotes autophagy-induced neuronal cell apoptosis by acting as a ceRNA for miR-485 to up-regulate ATG7 expression Yanbin Cao 1 & Lihua Pan 1 & Xuejun Zhang 1 & Wenbin Guo 1 & Dezhang Huang 2 Received: 21 April 2020 / Accepted: 11 August 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Long non-coding RNAs (lncRNAs) are bound up with various human diseases. However, their roles in brain ischemiareperfusion (I/R) injury remain largely unknown. This study aimed to reveal the potential mechanism of LncRNA SNHG3 on autophagy-induced neuronal cell apoptosis in the brain I/R injury. LncRNA SNHG3 and miR-485 or autophagy markers LC3II/I and Beclin-1 expressions were detected by qRT-PCR or Western blot and the apoptosis of N2a cells was analyzed by flow cytometry. Besides, the interactions between LncRNA SNHG3 and miR-485, miR-485 and ATG7 were validated by RNA pulldown and dual-luciferase reporter system assays. After the Oxygen and Glucose Deprivation (OGD) treatment of N2a cells transfected with pcDNA-SNHG3, pcDNA-SNHG3 + miR-485 mimic for 6 h, 1 mM autophagy inhibitor 3-MA was added and reoxygenated for 24 h, the effect of LncRNA SNHG3 on the autophagy-induced neuronal cell apoptosis was measured by Western blot and flow cytometry. LncRNA SNHG3 was highly expressed in the mouse model of transient middle cerebral artery occlusion and cell model of Oxygen and Glucose Deprivation/Reperfusion, while miR-485 was lowly expressed. Furthermore, miR-485 negatively regulated the luciferase activities of LncRNA SNHG3 and ATG7. After the OGD treatment of N2a cells transfected with pcDNA-SNHG3, pcDNA-SNHG3 + miR-485 mimic for 6 h, 1 mM 3-MA was added and reoxygenated for 24 h, the overexpression of LncRNA SNHG3 raised the ratio of LC3-II/LC3-I and Beclin-1 expression and boosted the apoptosis of N2a cells, while these effects were reversed after the transfection of miR-485 mimic. In general, our data expounded that the interference with LncRNA SNHG3 improved brain I/R injury by up-regulating miR-485 and down-regulating ATG7 to restrain autophagy and neuronal cell apoptosis. Keywords LncRNA SNHG3 . miR-485 . Autophagy . Neuronal . Apoptosis
Introduction Ischemic stroke, also known as cerebral infarction, is mainly caused by cerebral vascular occlusion and is one of the common causes of death and disability worldwide (Turner et al. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11011-020-00607-1) contains supplementary material, which is available to authorized users. * Dezhang Huang [email protected] 1
Department of Neurosurgery, Weihai municipal hospital, Weihai, Shandong, China
2
Department of Neurosurgery, Qilu Hospital (Qingdao), Cheeloo college of Medicine, Shandong University, No.758 Hefei Road, Qingdao 266035, Shandong Province, China
2013). Current major treatments for ischemic stroke include rapid revascularization, but the rapid recovery of cerebral blood supply may result in reperfusion injury (Duehrk
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