Follicle-stimulating hormone promotes age-related endometrial atrophy through cross-talk with transforming growth factor beta signal transduction pathway.
It is widely believed that endometrial atrophy in postmenopausal women is due to an age-related reduction in estrogen level. But the role of high circulating follicle-stimulating hormone (FSH) in postmenopausal syndrome is not clear. Here, we explored the role of high circulating FSH in physiological endometrial atrophy. We found that FSH exacerbated post-OVX endometrial atrophy in mice, and this effect was ameliorated by lowering FSH with Gonadotrophin-releasing hormone agonist (GnRHa). In vitro, FSH inhibited endometrial proliferation and promoted the apoptosis of primary cultured endometrial cells in a dose-dependent manner. In addition, upregulation of caspase3, caspase8, caspase9, autophagy-related proteins (ATG3, ATG5, ATG7, ATG12 and LC3) and downregulation of c-Jun were also observed in endometrial adenocytes. Furthermore, smad2 and smad3 showed a time-dependent activation in endometrial cells which can be partly inhibited by blocking the transforming growth factor beta receptor II (TβRII). In conclusion, FSH regulated endometrial atrophy by affecting the proliferation, autophagy and apoptosis of endometrial cells partly through activation of the transforming growth factor beta (TGFβ) pathway.
['Zhang|Dan|D|', 'Li|Jingyi|J|', 'Xu|Gufeng|G|', 'Zhang|Runjv|R|', 'Zhou|Chengliang|C|', 'Qian|Yeqing|Y|', 'Liu|Yifeng|Y|', 'Chen|Luting|L|', 'Zhu|Bo|B|', 'Ye|Xiaoqun|X|', 'Qu|Fan|F|', 'Liu|Xinmei|X|', 'Shi|Shuai|S|', 'Yang|Weijun|W|', 'Sheng|Jianzhong|J|', 'Huang|Hefeng|H|']
D000367:Age Factors D000818:Animals D001284:Atrophy D004195:Disease Models, Animal D004717:Endometrium D005260:Female D005640:Follicle Stimulating Hormone D006801:Humans D051379:Mice D015398:Signal Transduction D016212:Transforming Growth Factor beta
follicle-stimulating hormone atrophy transforming growth factor beta autophagy aging menopause