miR-351-5p/Miro2 axis contributes to hippocampal neural progenitor cell death via unbalanced mitochondrial fission
Ha Na Woo,Ha Na Woo,S. S. Park,Hae Lin Kim,Min Kyo Jung,Chan-Gi Pack,Jinsu Park,Yoonsuk Cho,Dong-Gyu Jo,Dong Kyu Kim,Inhee Mook-Jung,Seong Who Kim,Seong Who Kim,Heuiran Lee,Heuiran Lee +14 more
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TL;DR: In this article, miR-351-5p was shown to be a causative factor in hippocampal neural progenitor cell death through modulation of the mitochondrial guanosine triphosphatase (GTPase), Miro2.
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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 miR-351-5p-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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References
Autophagic cell death: Loch Ness monster or endangered species?
Han-Ming Shen,Patrice Codogno +1 more
TL;DR: This work proposes to define autophagic cell death as a modality of non-apoptotic or necrotic programmed cell death in which autophagy serves as a cell death mechanism, upon meeting the following set of criteria: cell death occurs without the involvement of apoptosis.
354
Miro proteins coordinate microtubule- and actin-dependent mitochondrial transport and distribution.
Guillermo López-Doménech,Christian Covill-Cooke,Davor Ivankovic,Els F. Halff,David F. Sheehan,Rosalind Norkett,Nicol Birsa,Josef T. Kittler +7 more
TL;DR: It is found that Miro is critical for recruiting and stabilising the mitochondrial myosin Myo19 on the mitochondria for coupling mitochondria to the actin cytoskeleton, to regulate key cellular functions such as cell proliferation.
274
MicroRNAs in neural development: from master regulators to fine-tuners.
Marek Rajman,Gerhard Schratt +1 more
TL;DR: An overview of the most prominent regulatory miRNAs that control neural development is provided, highlighting how they act as ‘master regulators’ or ‘fine-tuners’ of gene expression, depending on context, to influence processes such as cell fate determination, cell migration, neuronal polarization and synapse formation.
Evolving Concepts of Mitochondrial Dynamics.
TL;DR: In this article, the authors revisited mitochondrial dynamism with a fresh perspective developed from the recently discovered multifunctionality of mitochondrial fusion proteins and newly defined mechanisms for direct cross talk between mitochondrial dynamics, biogenesis, quality control, and trafficking pathways.
149
Miro phosphorylation sites regulate Parkin recruitment and mitochondrial motility.
TL;DR: It is proposed that the status of Miro phosphorylation influences the decision to undergo Parkin-dependent mitochondrial arrest, which, in the context of PINK1 action on other substrates, can restrict mitochondrial dynamics before mitophagy.
138