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β-Arrestin1/miR-326 Transcription Unit Is Epigenetically Regulated in Neural Stem Cells Where It Controls Stemness and Growth Arrest
Cell development is regulated by a complex network of mRNA-encoded proteins and microRNAs, all funnelling onto the modulation of self-renewal or differentiation genes. How intragenic microRNAs and their host genes are transcriptionally coregulated and their functional relationships for the control o...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5337365/ https://www.ncbi.nlm.nih.gov/pubmed/28298929 http://dx.doi.org/10.1155/2017/5274171 |
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author | Po, Agnese Begalli, Federica Abballe, Luana Alfano, Vincenzo Besharat, Zein Mersini Catanzaro, Giuseppina Vacca, Alessandra Napolitano, Maddalena Tafani, Marco Giangaspero, Felice Locatelli, Franco Ferretti, Elisabetta Miele, Evelina |
author_facet | Po, Agnese Begalli, Federica Abballe, Luana Alfano, Vincenzo Besharat, Zein Mersini Catanzaro, Giuseppina Vacca, Alessandra Napolitano, Maddalena Tafani, Marco Giangaspero, Felice Locatelli, Franco Ferretti, Elisabetta Miele, Evelina |
author_sort | Po, Agnese |
collection | PubMed |
description | Cell development is regulated by a complex network of mRNA-encoded proteins and microRNAs, all funnelling onto the modulation of self-renewal or differentiation genes. How intragenic microRNAs and their host genes are transcriptionally coregulated and their functional relationships for the control of neural stem cells (NSCs) are poorly understood. We propose here the intragenic miR-326 and its host gene β-arrestin1 as novel players whose epigenetic silencing maintains stemness in normal cerebellar stem cells. Such a regulation is mediated by CpG islands methylation of the common promoter. Epigenetic derepression of β-arrestin1/miR-326 by differentiation signals or demethylating agents leads to suppression of stemness features and cell growth and promotes cell differentiation. β-Arrestin1 inhibits cell proliferation by enhancing the nuclear expression of the cyclin-dependent kinase inhibitor p27. Therefore, we propose a new mechanism for the control of cerebellar NSCs where a coordinated epigenetic mechanism finely regulates β-arrestin1/miR-326 expression and consequently NSCs stemness and cell growth. |
format | Online Article Text |
id | pubmed-5337365 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-53373652017-03-15 β-Arrestin1/miR-326 Transcription Unit Is Epigenetically Regulated in Neural Stem Cells Where It Controls Stemness and Growth Arrest Po, Agnese Begalli, Federica Abballe, Luana Alfano, Vincenzo Besharat, Zein Mersini Catanzaro, Giuseppina Vacca, Alessandra Napolitano, Maddalena Tafani, Marco Giangaspero, Felice Locatelli, Franco Ferretti, Elisabetta Miele, Evelina Stem Cells Int Research Article Cell development is regulated by a complex network of mRNA-encoded proteins and microRNAs, all funnelling onto the modulation of self-renewal or differentiation genes. How intragenic microRNAs and their host genes are transcriptionally coregulated and their functional relationships for the control of neural stem cells (NSCs) are poorly understood. We propose here the intragenic miR-326 and its host gene β-arrestin1 as novel players whose epigenetic silencing maintains stemness in normal cerebellar stem cells. Such a regulation is mediated by CpG islands methylation of the common promoter. Epigenetic derepression of β-arrestin1/miR-326 by differentiation signals or demethylating agents leads to suppression of stemness features and cell growth and promotes cell differentiation. β-Arrestin1 inhibits cell proliferation by enhancing the nuclear expression of the cyclin-dependent kinase inhibitor p27. Therefore, we propose a new mechanism for the control of cerebellar NSCs where a coordinated epigenetic mechanism finely regulates β-arrestin1/miR-326 expression and consequently NSCs stemness and cell growth. Hindawi Publishing Corporation 2017 2017-02-12 /pmc/articles/PMC5337365/ /pubmed/28298929 http://dx.doi.org/10.1155/2017/5274171 Text en Copyright © 2017 Agnese Po et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Po, Agnese Begalli, Federica Abballe, Luana Alfano, Vincenzo Besharat, Zein Mersini Catanzaro, Giuseppina Vacca, Alessandra Napolitano, Maddalena Tafani, Marco Giangaspero, Felice Locatelli, Franco Ferretti, Elisabetta Miele, Evelina β-Arrestin1/miR-326 Transcription Unit Is Epigenetically Regulated in Neural Stem Cells Where It Controls Stemness and Growth Arrest |
title |
β-Arrestin1/miR-326 Transcription Unit Is Epigenetically Regulated in Neural Stem Cells Where It Controls Stemness and Growth Arrest |
title_full |
β-Arrestin1/miR-326 Transcription Unit Is Epigenetically Regulated in Neural Stem Cells Where It Controls Stemness and Growth Arrest |
title_fullStr |
β-Arrestin1/miR-326 Transcription Unit Is Epigenetically Regulated in Neural Stem Cells Where It Controls Stemness and Growth Arrest |
title_full_unstemmed |
β-Arrestin1/miR-326 Transcription Unit Is Epigenetically Regulated in Neural Stem Cells Where It Controls Stemness and Growth Arrest |
title_short |
β-Arrestin1/miR-326 Transcription Unit Is Epigenetically Regulated in Neural Stem Cells Where It Controls Stemness and Growth Arrest |
title_sort | β-arrestin1/mir-326 transcription unit is epigenetically regulated in neural stem cells where it controls stemness and growth arrest |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5337365/ https://www.ncbi.nlm.nih.gov/pubmed/28298929 http://dx.doi.org/10.1155/2017/5274171 |
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