MicroRNA-146a Promotes Oligodendrogenesis in Stroke
Recommended Citation
Liu XS, Chopp M, Pan WL, Wang XL, Fan BY, Zhang Y, Kassis H, Zhang RL, Zhang XM, and Zhang ZG. MicroRNA-146a promotes oligodendrogenesis in stroke. Mol Neurobiol 2017; 54(1):227-237.
Document Type
Article
Publication Date
1-1-2017
Publication Title
Molecular Neurobiology
Abstract
Stroke induces new myelinating oligodendrocytes that are involved in ischemic brain repair. Molecular mechanisms that regulate oligodendrogenesis have not been fully investigated. MicroRNAs (miRNAs) are small non-coding RNA molecules that post-transcriptionally regulate gene expression. MiR-146a has been reported to regulate immune response, but the role of miR-146a in oligodendrocyte progenitor cells (OPCs) remains unknown. Adult Wistar rats were subjected to the right middle cerebral artery occlusion (MCAo). In situ hybridization analysis with LNA probes against miR-146a revealed that stroke considerably increased miR-146a density in the corpus callosum and subventricular zone (SVZ) of the lateral ventricle of the ischemic hemisphere. In vitro, overexpression of miR-146a in neural progenitor cells (NPCs) significantly increased their differentiation into O4+ OPCs. Overexpression of miR-146a in primary OPCs increased their expression of myelin proteins, whereas attenuation of endogenous miR-146a suppressed generation of myelin proteins. MiR-146a also inversely regulated its target gene-IRAK1 expression in OPCs. Attenuation of IRAK1 in OPCs substantially increased myelin proteins and decreased OPC apoptosis. Collectively, our data suggest that miR-146a may mediate stroke-induced oligodendrogenesis.
Medical Subject Headings
Animals; Cell Differentiation; Cells, Cultured; Male; MicroRNAs; Myelin Proteins; Oligodendroglia; Rats; Rats, Wistar; Stroke
PubMed ID
26738853
Volume
54
Issue
1
First Page
227
Last Page
237
