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Cited 13 time in webofscience Cited 13 time in scopus
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miR-351-5p/Miro2 axis contributes to hippocampal neural progenitor cell death via unbalanced mitochondrial fission

Authors
Woo, Ha-NaPark, SujeongKim, Hae LinJung, Min-KyoPack, Chan-GiPark, JinsuCho, YoonsukJo, Dong-GyuKim, Dong KyuMook-Jung, InheeKim, Seong WhoLee, Heuiran
Issue Date
Mar-2021
Publisher
CELL PRESS
Citation
MOLECULAR THERAPY-NUCLEIC ACIDS, v.23, pp.643 - 656
Journal Title
MOLECULAR THERAPY-NUCLEIC ACIDS
Volume
23
Start Page
643
End Page
656
URI
http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/540
DOI
10.1016/j.omtn.2020.12.014
ISSN
2162-2531
Abstract
Adult hippocampal neurogenesis supports the structural and functional plasticity of the brain, while its decline is associated with neurodegeneration common in Alzheimer's disease (AD). Although the dysregulation of certain microRNAs (miRNAs) in AD have been observed, the effects of miRNAs on hippocampal neurogenesis are largely unknown. In this study, we demonstrated miR-351-5p as a causative factor in hippocampal neural progenitor cell death through modulation of the mitochondrial guanosine triphosphatase (GTPase), Miro2. Downregulation of Miro2 by siMiro2 induced cell death, similar to miR-351-5p, whereas ectopic Miro2 expression using an adenovirus abolished these effects. Excessively fragmented mitochondria and dysfunctional mitochondria were indexed by decreased mitochondrial potential, and increased reactive oxygen species were identified in miR351-5p-induced cell death. Moreover, subsequent induction of mitophagy via Pink1 and Parkin was observed in the presence of miR-351-5p and siMiro2. The suppression of mitochondrial fission by Mdivi-1 completely inhibited cell death by miR-351-5p. miR-351-5p expression increased whereas the level of Miro2 decreased in the hippocampus of AD model mice, emulating expression in AD patients. Collectively, the data indicate the mitochondrial fission and accompanying mitophagy by miR-351-5p/Miro2 axis as critical in hippocampal neural progenitor cell death, and a potential therapeutic target in AD.
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