表观遗传学
多囊卵巢
DNA甲基化
生物
转录组
甲基化
基因
生物信息学
内科学
内分泌学
遗传学
医学
基因表达
胰岛素抵抗
肥胖
作者
Nour El Houda Mimouni,Isabel Paiva,Anne‐Laure Barbotin,Fatima Ezzahra Timzoura,Damien Plassard,Stéphanie Le Gras,Gaëtan Ternier,Pascal Pigny,Sophie Catteau-Jonard,Virginie Simon,Vincent Prévot,Anne‐Laurence Boutillier,Paolo Giacobini
出处
期刊:Cell Metabolism
[Elsevier]
日期:2021-03-01
卷期号:33 (3): 513-530.e8
被引量:106
标识
DOI:10.1016/j.cmet.2021.01.004
摘要
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.
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