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Brain-derived neurotrophic factor promotes human granulosa-like tumor cell steroidogenesis and proliferation by activating the FSH receptor-mediated signaling pathway

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      Abstract

      Brain-derived neurotrophic factor (BDNF) and FSH receptor (FSHR) are expressed in ovarian granulosa cells, and play important roles in regulating follicle growth and oocyte maturation. Studies have linked the BDNF-associated signaling pathway to FSHR mRNA expression in the regulation of follicle development, but the mechanisms remain unknown. In the current study, we found that BDNF stimulated the secretion of estradiol and progesterone, and increased the proliferation of KGN cells (human granulosa-like tumor cell line). BDNF treatment also increased phosphorylated and ubiquitinated FSHR, and activated cAMP/PKA/CREB signaling pathway. Moreover, inhibition of BDNF expression by siRNA markedly reduced the estradiol secretion and down-regulated FSHR, aromatase and phosphorylated CREB; meanwhile, FSH treatment partly alleviated the effects of BDNF siRNA on KGN cells. These findings suggested that BDNF modulates graunlosa cell functions and the action probably mediated by FSHR-coupled signaling pathway, to affect aromatase-mediated steroidogenesis. These results provide an alternative target to optimize ovarian granulosa cell function.

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            Author and article information

            Affiliations
            [1 ]ISNI 0000 0001 2314 964X, GRID grid.41156.37, Center of Reproductive Medicine, Jinling Hospital, Clinical School of Medical College, , Nanjing University, ; Nanjing, Jiangsu People’s Republic of China
            [2 ]ISNI 0000 0001 2314 964X, GRID grid.41156.37, Department of Medical Statistics, Jinling Hospital, , Nanjing University, ; Nanjing, Jiangsu People’s Republic of China
            Contributors
            yaobing@nju.edu.cn
            Journal
            Sci Rep
            Sci Rep
            Scientific Reports
            Nature Publishing Group UK (London )
            2045-2322
            15 March 2017
            15 March 2017
            2017
            : 7
            28282971
            5428030
            203
            10.1038/s41598-017-00203-x
            © The Author(s) 2017

            This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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