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Type: Journal article
Title: Follicle-stimulating hormone promotes age-related endometrial atrophy through cross-talk with transforming growth factor beta signal transduction pathway
Author: Zhang, D.
Li, J.
Xu, G.
Zhang, R.
Zhou, C.
Qian, Y.
Liu, Y.
Chen, L.
Zhu, B.
Ye, X.
Qu, F.
Liu, X.
Shi, S.
Yang, W.
Sheng, J.
Huang, H.
Citation: Aging Cell, 2015; 14(2):284-287
Publisher: Elsevier
Issue Date: 2015
ISSN: 1474-9718
Statement of
Dan Zhang, Jingyi Li, Gufeng Xu, Runjv Zhang, Chengliang Zhou ... He-Feng Huang ... et al.
Abstract: 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.
Keywords: Aging; atrophy; autophagy; follicle‐stimulating hormone; menopause; transforming growth factor beta
Rights: © 2014 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
DOI: 10.1111/acel.12278
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