Intra-cellular mechanism of Anti-Müllerian hormone (AMH) in regulation of follicular development. (15th September 2016)

• Record Type: Journal Article
• Authors: Hayes, Emily; Kushnir, Vitaly; Ma, Xiaoting; Biswas, Anindita; Prizant, Hen; Gleicher, Norbert; Sen, Aritro
• Is Part Of: Molecular and cellular endocrinology. Volume 433(2016)
• Page Start: 56
• Page End: 65
• Publication Date: 2016-09-15
• Subjects: AMH -- FSH -- Follicular development -- miR-181a -- miR-181b; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2016.05.019
• Languages: English
• ISSNs: 0303-7207

Abstract

Abstract: Anti-Müllerian hormone (AMH) is a member of the transforming growth factor-β superfamily and plays a crucial role in testicular and ovarian functions. In clinical practice, AMH is used as a diagnostic and/or prognostic marker in women in association with ovulation induction and in various pathophysiological conditions. Despite widespread clinical use of AMH, our mechanistic understanding of AMH actions in regulating follicular development is limited. Using a mouse model, we in this study report that in vivo AMH treatment while stalls follicular development and inhibits ovulation, also prevents follicular atresia. We further show that these AMH actions are mediated through induction of two miRNAs, miR-181a and miR-181b, which regulate various aspects of FSH signaling and follicular growth, ultimately affecting downstream gene expression and folliculogenesis. We also report that in this mouse model AMH pre-treatment prior to superovulation improves oocyte yield. These studies, therefore, offer new mechanistic insight into AMH actions in folliculogenesis and point toward potential utilization of AMH as a therapeutic agent. Highlights: In vivo AMH treatment stalls folliculogenesis, and inhibits ovulation as well as ovarian gene expression. AMH inhibits FSH-induced follicular growth, aromatase expression and cAMP levels. AMH induces expression of miR-181a and miR-181b in granulosa cells. miR-181a and miR-181b target activin receptorIIa and adenylate cyclase 9. Exogenous AMH treatment enhances gonadotropin-induced ovulation in mice.