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MiR-202-5p attenuates neurological deficits and neuronal injury in MCAO model rats and OGD-induced injury in Neuro-2a cells by targeting eIF4E-mediated induction of autophagy and inhibition of Akt/GSK-3β pathway.

Abstract
Ischemic stroke is a common cerebrovascular disease caused by insufficient blood supply to the brain. In recent years, studies have demonstrated that microRNAs (miRNAs) are involved in a variety of biological processes in the nervous system. However, the effects of miR-202-5p on cerebral ischemic stroke injury have not been completely elucidated. In our study, N2a cells were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) treatment, and middle cerebral artery occlusion (MCAO) rat models were constructed. Our results indicated that decreased miR-202-5p expression was connected to N2a cells after OGD/R-induced injury and rats after MCAO. In addition, high miR-202-5p expression increased proliferation and prevented apoptosis and autophagy of OGD/R-treated N2a cells, while also effectively decreasing the infarct volume in MCAO model rats. We validated the interplay between miR-202-5p and eukaryotic translation initiation factor 4E (eIF4E), and found that miR-202-5p downregulated eIF4E by targeted combination. Moreover, we demonstrated that miR-202-5p accelerated proliferation and suppressed autophagy of OGD/R-induced N2a cells by targeting eIF4E. Meanwhile, our other results suggest that upregulation of miR-202-5p may activate the Akt/GSK-3β pathway in ischemic brain injury. Our findings suggest that miR-202-5p may serve as a protective agent for ischemia-reperfusion injury in stroke via eIF4E.
AuthorsBing Li, Zhi Huang, Ju Meng, Wenfeng Yu, Hua Yang
JournalMolecular and cellular probes (Mol Cell Probes) Vol. 51 Pg. 101497 (06 2020) ISSN: 1096-1194 [Electronic] England
PMID31877332 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.
Chemical References
  • Eukaryotic Initiation Factor-4E
  • LC3 protein, rat
  • MicroRNAs
  • Microtubule-Associated Proteins
  • Glycogen Synthase Kinase 3 beta
  • Proto-Oncogene Proteins c-akt
  • Glucose
Topics
  • Animals
  • Autophagosomes (genetics, metabolism, ultrastructure)
  • Autophagy (genetics)
  • Cell Hypoxia (genetics)
  • Cell Line
  • Cell Proliferation (genetics)
  • Disease Models, Animal
  • Down-Regulation
  • Eukaryotic Initiation Factor-4E (metabolism)
  • Glucose (deficiency)
  • Glycogen Synthase Kinase 3 beta (metabolism)
  • Infarction, Middle Cerebral Artery (genetics, metabolism)
  • Mice
  • MicroRNAs (genetics, metabolism)
  • Microscopy, Electron, Transmission
  • Microtubule-Associated Proteins (metabolism)
  • Neurons (metabolism)
  • Proto-Oncogene Proteins c-akt (metabolism)
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury (genetics, metabolism)
  • Signal Transduction (genetics)
  • Up-Regulation

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