miR-26b Promotes Granulosa Cell Apoptosis by Targeting ATM during Follicular Atresia in Porcine Ovary

More than 99% of ovarian follicles undergo atresia in mammals, but the mechanism of follicular atresia remains to be elucidated. In this study, we explored microRNA (miRNA) regulation of follicular atresia in porcine ovary. A miRNA expression profile was constructed for healthy, early atretic, and p...

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Detalles Bibliográficos
Autores principales: Lin, Fei, Li, Ran, Pan, Zeng xiang, Zhou, Bo, Yu, De bing, Wang, Xu guang, Ma, Xue shan, Han, Jing, Shen, Ming, Liu, Hong lin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2012
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3380909/
https://www.ncbi.nlm.nih.gov/pubmed/22737216
http://dx.doi.org/10.1371/journal.pone.0038640
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author Lin, Fei
Li, Ran
Pan, Zeng xiang
Zhou, Bo
Yu, De bing
Wang, Xu guang
Ma, Xue shan
Han, Jing
Shen, Ming
Liu, Hong lin
author_facet Lin, Fei
Li, Ran
Pan, Zeng xiang
Zhou, Bo
Yu, De bing
Wang, Xu guang
Ma, Xue shan
Han, Jing
Shen, Ming
Liu, Hong lin
author_sort Lin, Fei
collection PubMed
description More than 99% of ovarian follicles undergo atresia in mammals, but the mechanism of follicular atresia remains to be elucidated. In this study, we explored microRNA (miRNA) regulation of follicular atresia in porcine ovary. A miRNA expression profile was constructed for healthy, early atretic, and progressively atretic follicles, and the differentially expressed miRNAs were selected and analyzed. We found that miR-26b, which was upregulated during follicular atresia, increased the number of DNA breaks and promoted granulosa cell apoptosis by targeting the ataxia telangiectasia mutated gene directly in vitro.
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spelling pubmed-33809092012-06-26 miR-26b Promotes Granulosa Cell Apoptosis by Targeting ATM during Follicular Atresia in Porcine Ovary Lin, Fei Li, Ran Pan, Zeng xiang Zhou, Bo Yu, De bing Wang, Xu guang Ma, Xue shan Han, Jing Shen, Ming Liu, Hong lin PLoS One Research Article More than 99% of ovarian follicles undergo atresia in mammals, but the mechanism of follicular atresia remains to be elucidated. In this study, we explored microRNA (miRNA) regulation of follicular atresia in porcine ovary. A miRNA expression profile was constructed for healthy, early atretic, and progressively atretic follicles, and the differentially expressed miRNAs were selected and analyzed. We found that miR-26b, which was upregulated during follicular atresia, increased the number of DNA breaks and promoted granulosa cell apoptosis by targeting the ataxia telangiectasia mutated gene directly in vitro. Public Library of Science 2012-06-21 /pmc/articles/PMC3380909/ /pubmed/22737216 http://dx.doi.org/10.1371/journal.pone.0038640 Text en Lin et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Lin, Fei
Li, Ran
Pan, Zeng xiang
Zhou, Bo
Yu, De bing
Wang, Xu guang
Ma, Xue shan
Han, Jing
Shen, Ming
Liu, Hong lin
miR-26b Promotes Granulosa Cell Apoptosis by Targeting ATM during Follicular Atresia in Porcine Ovary
title miR-26b Promotes Granulosa Cell Apoptosis by Targeting ATM during Follicular Atresia in Porcine Ovary
title_full miR-26b Promotes Granulosa Cell Apoptosis by Targeting ATM during Follicular Atresia in Porcine Ovary
title_fullStr miR-26b Promotes Granulosa Cell Apoptosis by Targeting ATM during Follicular Atresia in Porcine Ovary
title_full_unstemmed miR-26b Promotes Granulosa Cell Apoptosis by Targeting ATM during Follicular Atresia in Porcine Ovary
title_short miR-26b Promotes Granulosa Cell Apoptosis by Targeting ATM during Follicular Atresia in Porcine Ovary
title_sort mir-26b promotes granulosa cell apoptosis by targeting atm during follicular atresia in porcine ovary
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3380909/
https://www.ncbi.nlm.nih.gov/pubmed/22737216
http://dx.doi.org/10.1371/journal.pone.0038640
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