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Connexin26 gap junction mediates miRNA intercellular genetic communication in the cochlea and is required for inner ear development

Organ development requires well-established intercellular communication to coordinate cell proliferations and differentiations. MicroRNAs (miRNAs) are small, non-coding RNAs that can broadly regulate gene expression and play a critical role in the organ development. In this study, we found that miRN...

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Autores principales: Zhu, Yan, Zong, Liang, Mei, Ling, Zhao, Hong-Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4614881/
https://www.ncbi.nlm.nih.gov/pubmed/26490746
http://dx.doi.org/10.1038/srep15647
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author Zhu, Yan
Zong, Liang
Mei, Ling
Zhao, Hong-Bo
author_facet Zhu, Yan
Zong, Liang
Mei, Ling
Zhao, Hong-Bo
author_sort Zhu, Yan
collection PubMed
description Organ development requires well-established intercellular communication to coordinate cell proliferations and differentiations. MicroRNAs (miRNAs) are small, non-coding RNAs that can broadly regulate gene expression and play a critical role in the organ development. In this study, we found that miRNAs could pass through gap junctions between native cochlear supporting cells to play a role in the cochlear development. Connexin26 (Cx26) and Cx30 are predominant isoforms and co-express in the cochlea. Cx26 deficiency but not Cx30 deficiency can cause cochlear developmental disorders. We found that associated with Cx26 deletion induced the cochlear developmental disorders, deletion of Cx26 but not Cx30 disrupted miRNA intercellular transfer in the cochlea, although inner ear gap junctions still retained permeability after deletion of Cx26. Moreover, we found that deletion of Cx26 but not Cx30 reduced miR-96 expression in the cochlea during postnatal development. The reduction is associated with the cochlear tunnel developmental disorder in Cx26 knockout (KO) mice. These data reveal that Cx26-mediated intercellular communication is required for cochlear development and that deficiency of Cx26 can impair miRNA-mediated intercellular genetic communication in the cochlea, which may lead to cochlear developmental disorders and eventually congenital deafness as previously reported.
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spelling pubmed-46148812015-10-29 Connexin26 gap junction mediates miRNA intercellular genetic communication in the cochlea and is required for inner ear development Zhu, Yan Zong, Liang Mei, Ling Zhao, Hong-Bo Sci Rep Article Organ development requires well-established intercellular communication to coordinate cell proliferations and differentiations. MicroRNAs (miRNAs) are small, non-coding RNAs that can broadly regulate gene expression and play a critical role in the organ development. In this study, we found that miRNAs could pass through gap junctions between native cochlear supporting cells to play a role in the cochlear development. Connexin26 (Cx26) and Cx30 are predominant isoforms and co-express in the cochlea. Cx26 deficiency but not Cx30 deficiency can cause cochlear developmental disorders. We found that associated with Cx26 deletion induced the cochlear developmental disorders, deletion of Cx26 but not Cx30 disrupted miRNA intercellular transfer in the cochlea, although inner ear gap junctions still retained permeability after deletion of Cx26. Moreover, we found that deletion of Cx26 but not Cx30 reduced miR-96 expression in the cochlea during postnatal development. The reduction is associated with the cochlear tunnel developmental disorder in Cx26 knockout (KO) mice. These data reveal that Cx26-mediated intercellular communication is required for cochlear development and that deficiency of Cx26 can impair miRNA-mediated intercellular genetic communication in the cochlea, which may lead to cochlear developmental disorders and eventually congenital deafness as previously reported. Nature Publishing Group 2015-10-22 /pmc/articles/PMC4614881/ /pubmed/26490746 http://dx.doi.org/10.1038/srep15647 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Zhu, Yan
Zong, Liang
Mei, Ling
Zhao, Hong-Bo
Connexin26 gap junction mediates miRNA intercellular genetic communication in the cochlea and is required for inner ear development
title Connexin26 gap junction mediates miRNA intercellular genetic communication in the cochlea and is required for inner ear development
title_full Connexin26 gap junction mediates miRNA intercellular genetic communication in the cochlea and is required for inner ear development
title_fullStr Connexin26 gap junction mediates miRNA intercellular genetic communication in the cochlea and is required for inner ear development
title_full_unstemmed Connexin26 gap junction mediates miRNA intercellular genetic communication in the cochlea and is required for inner ear development
title_short Connexin26 gap junction mediates miRNA intercellular genetic communication in the cochlea and is required for inner ear development
title_sort connexin26 gap junction mediates mirna intercellular genetic communication in the cochlea and is required for inner ear development
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4614881/
https://www.ncbi.nlm.nih.gov/pubmed/26490746
http://dx.doi.org/10.1038/srep15647
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