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The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders
miR-17 ~ 92, an miRNA family containing three paralogous polycistronic clusters, was initially considered as an oncogene and was later demonstrated to trigger various physiological and pathological processes. Emerging evidence has implicated miR-17 ~ 92 family as a master regulator of neurogenesis....
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8930872/ https://www.ncbi.nlm.nih.gov/pubmed/33030674 http://dx.doi.org/10.1007/s12015-020-10050-5 |
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author | Xia, Xiaohuan Wang, Yi Zheng, Jialin C. |
author_facet | Xia, Xiaohuan Wang, Yi Zheng, Jialin C. |
author_sort | Xia, Xiaohuan |
collection | PubMed |
description | miR-17 ~ 92, an miRNA family containing three paralogous polycistronic clusters, was initially considered as an oncogene and was later demonstrated to trigger various physiological and pathological processes. Emerging evidence has implicated miR-17 ~ 92 family as a master regulator of neurogenesis. Through targeting numerous genes that affect cell cycle arrest, stemness deprivation, and lineage commitment, miR-17 ~ 92 family controls the proliferation and neuronal differentiation of neural stem/progenitor cells in both developmental and adult brains. Due to the essential roles of miR-17 ~ 92 family, its misexpression is widely associated with acute and chronic neurological disorders by attenuating neurogenesis and facilitating neuronal apoptosis. The promising neurogenic potential of miR-17 ~ 92 family also makes it a promising “medicine” to activate the endogenous and exogenous regenerative machinery, thus enhance tissue repair and function recovery after brain injury. In this review, we focus on the recent progress made toward understanding the involvement of miR-17 ~ 92 family in regulating both developmental and adult neurogenesis, and discuss the regenerative potential of miR-17 ~ 92 family in treating neurological disorders. [Figure: see text] |
format | Online Article Text |
id | pubmed-8930872 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-89308722022-04-01 The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders Xia, Xiaohuan Wang, Yi Zheng, Jialin C. Stem Cell Rev Rep Article miR-17 ~ 92, an miRNA family containing three paralogous polycistronic clusters, was initially considered as an oncogene and was later demonstrated to trigger various physiological and pathological processes. Emerging evidence has implicated miR-17 ~ 92 family as a master regulator of neurogenesis. Through targeting numerous genes that affect cell cycle arrest, stemness deprivation, and lineage commitment, miR-17 ~ 92 family controls the proliferation and neuronal differentiation of neural stem/progenitor cells in both developmental and adult brains. Due to the essential roles of miR-17 ~ 92 family, its misexpression is widely associated with acute and chronic neurological disorders by attenuating neurogenesis and facilitating neuronal apoptosis. The promising neurogenic potential of miR-17 ~ 92 family also makes it a promising “medicine” to activate the endogenous and exogenous regenerative machinery, thus enhance tissue repair and function recovery after brain injury. In this review, we focus on the recent progress made toward understanding the involvement of miR-17 ~ 92 family in regulating both developmental and adult neurogenesis, and discuss the regenerative potential of miR-17 ~ 92 family in treating neurological disorders. [Figure: see text] Springer US 2020-10-08 2022 /pmc/articles/PMC8930872/ /pubmed/33030674 http://dx.doi.org/10.1007/s12015-020-10050-5 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Xia, Xiaohuan Wang, Yi Zheng, Jialin C. The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders |
title | The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders |
title_full | The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders |
title_fullStr | The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders |
title_full_unstemmed | The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders |
title_short | The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders |
title_sort | microrna-17 ~ 92 family as a key regulator of neurogenesis and potential regenerative therapeutics of neurological disorders |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8930872/ https://www.ncbi.nlm.nih.gov/pubmed/33030674 http://dx.doi.org/10.1007/s12015-020-10050-5 |
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