Metformin improves epigenetic modification involved in oocyte growth and embryo development in polycystic ovary syndrome mice model
The possible relationship between dehydroepiandrosterone (DHEA)‐induced polycystic ovary syndrome (PCOS) and epigenetic changes (ECs) leading to the impaired oocyte quality, has not been investigated yet. So, this study aimed to provide an insight into the relationship of the impaired oocyte quality...
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Published in | Molecular reproduction and development Vol. 88; no. 12; pp. 817 - 829 |
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Abstract | The possible relationship between dehydroepiandrosterone (DHEA)‐induced polycystic ovary syndrome (PCOS) and epigenetic changes (ECs) leading to the impaired oocyte quality, has not been investigated yet. So, this study aimed to provide an insight into the relationship of the impaired oocyte quality with ECs in a mice DHEA‐induced PCOS model and to further reveal the effect of metformin treatment. For this purpose, 80 female BALB/C mice were randomly divided into four equal groups, named as the control, sham, (DHEA) and DHEA + Metformin groups. The alterations in acetylation of H4K5 and H4K16, and in methylation of DNA (5MeC) and H3K9 were evaluated using immunocytochemical. Moreover, the expression of Hdac1, Hdac2, Dnmt1, and Dnmt3a genes involved in ECs were analyzed using reverse‐transcription polymerase chain reaction. As well, the levels of mitochondrial membrane potential (MMP), oxidative stress (OS), embryo development, ovarian morphology, sexual hormone, ovulatory function, and AMPKα phosphorylation activity were compared in all the studied groups. Metformin attenuated the damages induced by DHEA as indicated by the normalized the estrous cycle, the improved ovarian morphology, the decreased sexual hormone and OS levels, and the increased MMP and AMPKα phosphorylation levels. In the metformin group, the Dnmt1, Dnmt3a, and Hdac2 genes have significantly upregulated compared to the DHEA group. However, metformin was found to have no effect on the expression level of Hdac1. In this regard, significant decrease and increase were observed in both the acetylated H4K16 and methylated H3K9 within MII oocytes in the DHEA + Metformin group compared with the DHEA group. Our results show that metformin could enhance the developmental competence of PCOS oocytes via reducing OS and ECs. |
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AbstractList | The possible relationship between dehydroepiandrosterone (DHEA)-induced polycystic ovary syndrome (PCOS) and epigenetic changes (ECs) leading to the impaired oocyte quality, has not been investigated yet. So, this study aimed to provide an insight into the relationship of the impaired oocyte quality with ECs in a mice DHEA-induced PCOS model and to further reveal the effect of metformin treatment. For this purpose, 80 female BALB/C mice were randomly divided into four equal groups, named as the control, sham, (DHEA) and DHEA + Metformin groups. The alterations in acetylation of H4K5 and H4K16, and in methylation of DNA (5MeC) and H3K9 were evaluated using immunocytochemical. Moreover, the expression of Hdac1, Hdac2, Dnmt1, and Dnmt3a genes involved in ECs were analyzed using reverse-transcription polymerase chain reaction. As well, the levels of mitochondrial membrane potential (MMP), oxidative stress (OS), embryo development, ovarian morphology, sexual hormone, ovulatory function, and AMPKα phosphorylation activity were compared in all the studied groups. Metformin attenuated the damages induced by DHEA as indicated by the normalized the estrous cycle, the improved ovarian morphology, the decreased sexual hormone and OS levels, and the increased MMP and AMPKα phosphorylation levels. In the metformin group, the Dnmt1, Dnmt3a, and Hdac2 genes have significantly upregulated compared to the DHEA group. However, metformin was found to have no effect on the expression level of Hdac1. In this regard, significant decrease and increase were observed in both the acetylated H4K16 and methylated H3K9 within MII oocytes in the DHEA + Metformin group compared with the DHEA group. Our results show that metformin could enhance the developmental competence of PCOS oocytes via reducing OS and ECs. Abstract The possible relationship between dehydroepiandrosterone (DHEA)‐induced polycystic ovary syndrome (PCOS) and epigenetic changes (ECs) leading to the impaired oocyte quality, has not been investigated yet. So, this study aimed to provide an insight into the relationship of the impaired oocyte quality with ECs in a mice DHEA‐induced PCOS model and to further reveal the effect of metformin treatment. For this purpose, 80 female BALB/C mice were randomly divided into four equal groups, named as the control, sham, (DHEA) and DHEA + Metformin groups. The alterations in acetylation of H4K5 and H4K16, and in methylation of DNA (5MeC) and H3K9 were evaluated using immunocytochemical. Moreover, the expression of Hdac1, Hdac2, Dnmt1, and Dnmt3a genes involved in ECs were analyzed using reverse‐transcription polymerase chain reaction. As well, the levels of mitochondrial membrane potential (MMP), oxidative stress (OS), embryo development, ovarian morphology, sexual hormone, ovulatory function, and AMPKα phosphorylation activity were compared in all the studied groups. Metformin attenuated the damages induced by DHEA as indicated by the normalized the estrous cycle, the improved ovarian morphology, the decreased sexual hormone and OS levels, and the increased MMP and AMPKα phosphorylation levels. In the metformin group, the Dnmt1 , Dnmt3a , and Hdac 2 genes have significantly upregulated compared to the DHEA group. However, metformin was found to have no effect on the expression level of Hdac1 . In this regard, significant decrease and increase were observed in both the acetylated H4K16 and methylated H3K9 within MII oocytes in the DHEA + Metformin group compared with the DHEA group. Our results show that metformin could enhance the developmental competence of PCOS oocytes via reducing OS and ECs. |
Author | Aryanpour, Roya Salahi, Elnaz Amidi, Fardin Amani Abkenari, Showra Safdarian, Leili Sobhani, Aligholi Hosseini, Ali |
Author_xml | – sequence: 1 givenname: Showra surname: Amani Abkenari fullname: Amani Abkenari, Showra organization: Tehran University of Medical Sciences – sequence: 2 givenname: Leili surname: Safdarian fullname: Safdarian, Leili organization: Tehran University of Medical Sciences – sequence: 3 givenname: Fardin surname: Amidi fullname: Amidi, Fardin organization: Tehran University of Medical Sciences – sequence: 4 givenname: Ali surname: Hosseini fullname: Hosseini, Ali organization: Shahid Beheshti University of Medical Sciences – sequence: 5 givenname: Roya surname: Aryanpour fullname: Aryanpour, Roya organization: Yasuj University of Medical Science – sequence: 6 givenname: Elnaz surname: Salahi fullname: Salahi, Elnaz organization: Tehran University of Medical Sciences – sequence: 7 givenname: Aligholi surname: Sobhani fullname: Sobhani, Aligholi email: sobhania@sina.tums.ac.ir organization: Tehran University of Medical Sciences |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34658106$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_3390_ijms241713357 crossref_primary_10_1002_mrd_23720 crossref_primary_10_3390_ijms24076857 crossref_primary_10_1007_s43032_022_00869_3 crossref_primary_10_1093_biolre_ioac051 crossref_primary_10_1186_s10020_022_00446_z crossref_primary_10_4103_jhrs_jhrs_64_22 crossref_primary_10_1016_j_reprotox_2022_04_010 crossref_primary_10_2147_IJN_S360000 crossref_primary_10_3390_medicina57111251 crossref_primary_10_3389_fendo_2023_1245719 |
Cites_doi | 10.1016/j.biochi.2015.06.019 10.1186/1477-7827-4-16 10.1038/srep18858 10.1210/er.2002-0015 10.1016/j.repbio.2019.07.002 10.1155/2016/8589318 10.3390/nu10091137 10.1016/j.bbagrm.2014.02.007 10.1371/journal.pone.0119680 10.4161/cc.28189 10.1186/1477-7827-10-49 10.1111/dom.13262 10.1016/j.repbio.2020.02.005 10.1038/cdd.2016.31 10.1016/S1472-6483(10)60038-7 10.1186/s12943-017-0648-1 10.1210/en.2002-220182 10.1371/journal.pone.0122370 10.2337/diabetes.51.7.2074 10.1016/j.repbio.2019.09.006 10.1080/19396368.2018.1480076 10.1371/journal.pone.0127512 10.3109/19396368.2010.482726 10.1016/j.fertnstert.2013.10.041 10.1677/joe.0.1550233 10.1080/19396368.2017.1410591 10.3389/fendo.2018.00675 10.2337/db18-0537 10.1097/00006250-200304000-00029 10.1095/biolreprod64.2.696 10.1016/j.placenta.2008.08.009 10.1038/s41598-019-53286-z 10.4161/cc.9.10.11599 10.3390/genes8060148 10.1016/j.ydbio.2013.01.015 |
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Keywords | acetylation metformin dehydroepiandrosterone methylation |
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Snippet | The possible relationship between dehydroepiandrosterone (DHEA)‐induced polycystic ovary syndrome (PCOS) and epigenetic changes (ECs) leading to the impaired... The possible relationship between dehydroepiandrosterone (DHEA)-induced polycystic ovary syndrome (PCOS) and epigenetic changes (ECs) leading to the impaired... Abstract The possible relationship between dehydroepiandrosterone (DHEA)‐induced polycystic ovary syndrome (PCOS) and epigenetic changes (ECs) leading to the... |
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SubjectTerms | Acetylation Animals Antidiabetics Dehydroepiandrosterone Dehydroepiandrosterone - adverse effects DNA methylation DNMT1 protein Embryonic Development Epigenesis, Genetic Epigenetics Estrus cycle Female HDAC2 protein Histone deacetylase Membrane potential Metformin Metformin - pharmacology methylation Mice Mice, Inbred BALB C Mitochondria Morphology Oocytes Oocytes - metabolism Ovaries Oxidative stress Phosphorylation Polycystic ovary syndrome Polycystic Ovary Syndrome - chemically induced Polycystic Ovary Syndrome - genetics Polycystic Ovary Syndrome - metabolism Polymerase chain reaction |
Title | Metformin improves epigenetic modification involved in oocyte growth and embryo development in polycystic ovary syndrome mice model |
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