Li-Xia Dong1, Hai-Lan Bao1, Yan-Yun Zhang1, Yu Liu1, Guo-Wei Zhang2, Feng-Mao An3. 1. College of Nursing, Inner Mongolia University for Nationalities, Tongliao, 028000, Inner Mongolia Autonomous Region, PR China; Institute of Dementia, Inner Mongolia University for Nationalities, Tongliao, 028002, Inner Mongolia, PR China. 2. College of Nursing, Inner Mongolia University for Nationalities, Tongliao, 028000, Inner Mongolia Autonomous Region, PR China; Institute of Dementia, Inner Mongolia University for Nationalities, Tongliao, 028002, Inner Mongolia, PR China. Electronic address: ZHangGuoWeiGW2222@outlook.com. 3. Institute of Dementia, Inner Mongolia University for Nationalities, Tongliao, 028002, Inner Mongolia, PR China; Inner Mongolia Key Laboratory of Mongolian Medicine Pharmacology for Cardio-Cerebral Vascular System, Tongliao, 028002, Inner Mongolia, PR China. Electronic address: Anfengmao89898@163.com.
Abstract
OBJECTIVE: Studies have focused on the functions of microRNAs (miRNAs) in Alzheimer's disease (AD), but not much on miR-16-5p. Hence, this study intends to unearth the mechanism of AD, mainly focusing on miR-16-5p/B-cell translocation gene 2 (BTG2) axis. METHODS: APPswe/PS1dE9 mice were injected with depleted BTG2 and/or restored miR-16-5p vectors into the third ventricle to explore their roles in neurological function, neuronal damage, autophagy and apoptosis in AD mice. In vitro cultured hippocampal neurons were transfected with depleted BTG2 and/or restored miR-16-5p vector to interpret their functions in neuronal viability and apoptosis. MiR-16-5p and BTG2 expression in hippocampal tissues and neurons were detected. RESULTS: Lower miR-16-5p and higher BTG2 expression levels were found in hippocampal tissues and neurons. MiR-16-5p up-regulation or BTG2 down-regulation improved neurological function and neuronal damage and inhibited neuronal autophagy and apoptosis in AD mice. Restored miR-16-5p or depleted BTG2 restrained neuronal viability and apoptosis in vitro. CONCLUSION: Our study reveals that restored miR-16-5p or depleted BTG2 protects neurological function and suppresses neuronal autophagy and apoptosis in AD mice, which renews a novel guide toward AD treatments from the perspective of miR-16-5p/BTG2 axis.
OBJECTIVE: Studies have focused on the functions of microRNAs (miRNAs) in Alzheimer's disease (AD), but not much on miR-16-5p. Hence, this study intends to unearth the mechanism of AD, mainly focusing on miR-16-5p/B-cell translocation gene 2 (BTG2) axis. METHODS: APPswe/PS1dE9 mice were injected with depleted BTG2 and/or restored miR-16-5p vectors into the third ventricle to explore their roles in neurological function, neuronal damage, autophagy and apoptosis in AD mice. In vitro cultured hippocampal neurons were transfected with depleted BTG2 and/or restored miR-16-5p vector to interpret their functions in neuronal viability and apoptosis. MiR-16-5p and BTG2 expression in hippocampal tissues and neurons were detected. RESULTS: Lower miR-16-5p and higher BTG2 expression levels were found in hippocampal tissues and neurons. MiR-16-5p up-regulation or BTG2 down-regulation improved neurological function and neuronal damage and inhibited neuronal autophagy and apoptosis in AD mice. Restored miR-16-5p or depleted BTG2 restrained neuronal viability and apoptosis in vitro. CONCLUSION: Our study reveals that restored miR-16-5p or depleted BTG2 protects neurological function and suppresses neuronal autophagy and apoptosis in AD mice, which renews a novel guide toward AD treatments from the perspective of miR-16-5p/BTG2 axis.
Authors: Ma'mon M Hatmal; Mohammad A I Al-Hatamleh; Amin N Olaimat; Walhan Alshaer; Hanan Hasan; Khaled A Albakri; Enas Alkhafaji; Nada N Issa; Murad A Al-Holy; Salim M Abderrahman; Atiyeh M Abdallah; Rohimah Mohamud Journal: Biomedicines Date: 2022-05-24