| Literature DB >> 33539777 |
Nour El Houda Mimouni1, Isabel Paiva2, Anne-Laure Barbotin1, Fatima Ezzahra Timzoura1, Damien Plassard3, Stephanie Le Gras3, Gaetan Ternier1, Pascal Pigny4, Sophie Catteau-Jonard5, Virginie Simon5, Vincent Prevot1, Anne-Laurence Boutillier6, Paolo Giacobini7.
Abstract
Polycystic ovary syndrome (PCOS) is the most common reproductive and metabolic disorder affecting women of reproductive age. PCOS has a strong heritable component, but its pathogenesis has been unclear. Here, we performed RNA sequencing and genome-wide DNA methylation profiling of ovarian tissue from control and third-generation PCOS-like mice. We found that DNA hypomethylation regulates key genes associated with PCOS and that several of the differentially methylated genes are also altered in blood samples from women with PCOS compared with healthy controls. Based on this insight, we treated the PCOS mouse model with the methyl group donor S-adenosylmethionine and found that it corrected their transcriptomic, neuroendocrine, and metabolic defects. These findings show that the transmission of PCOS traits to future generations occurs via an altered landscape of DNA methylation and propose methylome markers as a possible diagnostic landmark for the condition, while also identifying potential candidates for epigenetic-based therapy.Entities:
Keywords: AMH; PCOS; developmental programming; epigenetics; fertility; inheritance; metabolic disorder; methylation; neuroendocrine; transgenerational
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Year: 2021 PMID: 33539777 PMCID: PMC7928942 DOI: 10.1016/j.cmet.2021.01.004
Source DB: PubMed Journal: Cell Metab ISSN: 1550-4131 Impact factor: 27.287