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.
|
Authors | Bing Li, Zhi Huang, Ju Meng, Wenfeng Yu, Hua Yang |
Journal | Molecular and cellular probes
(Mol Cell Probes)
Vol. 51
Pg. 101497
(06 2020)
ISSN: 1096-1194 [Electronic] England |
PMID | 31877332
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
|
Copyright | Copyright © 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
|