FSH-induced p38-MAPK-mediated dephosphorylation at serine 727 of the signal transducer and activator of transcription 1 decreases Cyp1b1 expression in mouse granulosa cells
作者： Xue-Hai Du , Xiao-Long Zhou , Rui Cao , Peng Xiao , Yun Teng
DOI: 10.1016/J.CELLSIG.2014.10.002
关键词:
摘要: Most mammalian follicles undergo atresia at various stages before ovulation, and granulosa cell apoptosis is a major cause of antral follicular atresia. Estradiol an essential mitogen for proliferation in vivo inhibition apoptosis. The estradiol-producing capacity metabolism levels are important follicle health, sufficient estradiol necessary development ovulation. Cyp1b1, member the cytochrome P450 1 subfamily, responsible wide variety halogenated polycyclic aromatic hydrocarbons diverse tissues. In mouse follicles, Cyp1b1 converts to 4-hydroxyestradiol. We investigated cells (MGCs) vitro found that played crucial role dominant follicles. Follicle-stimulating hormone (FSH) decreased estrogen by reducing mRNA protein MGCs. Furthermore, FSH regulated signal transducer activator transcription (STAT1), significant factor mediating dephosphorylation STAT1 on serine 727 (Ser(727)) p38 mitogen-activated kinase (MAPK) may be involved FSH-induced Ser(727) These results suggested functions via MAPK-induced downregulate expression maintain
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