Regulation of miRNA 219 and miRNA Clusters 338 and 17-92 in Oligodendrocytes
MicroRNAs (miRs) regulate diverse molecular and cellular processes including oligodendrocyte (OL) precursor cell (OPC) proliferation and differentiation in rodents. However, the role of miRs in human OPCs is poorly understood. To identify miRs that may regulate these processes in humans, we isolated...
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Published in | Frontiers in genetics Vol. 3; p. 46 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Research Foundation
2012
Frontiers Media S.A |
Subjects | |
Online Access | Get full text |
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Summary: | MicroRNAs (miRs) regulate diverse molecular and cellular processes including oligodendrocyte (OL) precursor cell (OPC) proliferation and differentiation in rodents. However, the role of miRs in human OPCs is poorly understood. To identify miRs that may regulate these processes in humans, we isolated OL lineage cells from human white matter and analyzed their miR profile. Using endpoint RT-PCR assays and quantitative real-time PCR, we demonstrate that miR-219, miR-338, and miR-17-92 are enriched in human white matter and expressed in acutely isolated human OLs. In addition, we report the expression of closely related miRs (miR-219-1-3p, miR-219-2-3p, miR-1250, miR-657, miR-3065-5p, miR-3065-3p) in both rodent and human OLs. Our findings demonstrate that miRs implicated in rodent OPC proliferation and differentiation are regulated in human OLs and may regulate myelination program in humans. Thus, these miRs should be recognized as potential therapeutic targets in demyelinating disorders. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 This article was submitted to Frontiers in Non-Coding RNA, a specialty of Frontiers in Genetics. Edited by: Peng Jin, Emory University School of Medicine, USA Reviewed by: Yanan Yang, MD Anderson Cancer Center, USA; Bruce Trapp, Cleveland Clinic, USA |
ISSN: | 1664-8021 1664-8021 |
DOI: | 10.3389/fgene.2012.00046 |