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      Expression of the gonadotropin receptors during follicular development

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          Abstract

          Background

          Gonadotropins induce follicular development that leads to ovulation and luteinization. In women, the level of gonadotropins, along with the expression of their receptors, changes dynamically throughout the menstrual cycle. This study aimed to clarify the mechanisms underlying these phenomena.

          Methods

          The literature was reviewed, including that published by the authors.

          Main findings (Results)

          Follicle‐stimulating hormone receptor expression in the granulosa cells was induced by androgens that were derived from growth differentiation factor‐9‐stimulated theca cells. In the theca cells, luteinizing hormone receptor ( LHR) expression was noted from their appearance. In the granulosa cells, follicle‐stimulating hormone ( FSH) stimulation was essential for LHR expression. However, FSH alone was not sufficient to respond to the luteinizing hormone ( LH) surge for oocyte maturation, ovulation, and subsequent luteinization. To achieve these stages, various local factors that were derived from the granulosa and theca cells in response to FSH and LH stimulation had to work synergistically in an autocrine/paracrine manner to strongly induce LHR expression. Following the LH surge, the LHR expression decreased markedly; mi RNAs were involved in this transient LHR downregulation. Following ovulation, LHR expression drastically increased again toward luteinization.

          Conclusion

          The expression of gonadotropin receptors is controlled by sophisticated and complicated systems; a breakdown of this system could lead to ovulation disorders.

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          Most cited references66

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          Interleukin-6 family of cytokines and gp130.

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            Androgens stimulate early stages of follicular growth in the primate ovary.

            The concept that androgens are atretogenic, derived from murine ovary studies, is difficult to reconcile with the fact that hyperandrogenic women have more developing follicles than normal-cycling women. To evaluate androgen's effects on primate follicular growth and survival, normal-cycling rhesus monkeys were treated with placebo-, testosterone-(T), or dihydrotestosterone-sustained release implants, and ovaries were taken for histological analysis after 3-10 d of treatment. Growing preantral and small antral follicles up to 1 mm in diameter were significantly and progressively increased in number and thecal layer thickness in T-treated monkeys from 3-10 d. Granulosa and thecal cell proliferation, as determined by immunodetection of the Ki67 antigen, were significantly increased in these follicles. Preovulatory follicles (> 1 mm), however, were not increased in number in androgen-treated animals. Follicular atresia was not increased and there were actually significantly fewer apoptotic granulosa cells in the T-treated groups. Dihydrotestosterone treatment had identical effects, indicating that these growth-promoting actions are mediated by the androgen receptor. These findings show that, over the short term at least, androgens are not atretogenic and actually enhance follicular growth and survival in the primate. These new data provide a plausible explanation for the pathogenesis of "polycystic" ovaries in hyperandrogenism.
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              The lutropin/choriogonadotropin receptor, a 2002 perspective.

              Reproduction cannot take place without the proper functioning of the lutropin/choriogonadotropin receptor (LHR). When the LHR does not work properly, ovulation does not occur in females and Leydig cells do not develop normally in the male. Also, because the LHR is essential for sustaining the elevated levels of progesterone needed to maintain pregnancy during the first trimester, disruptions in the functions of the LHR during pregnancy have catastrophic consequences. As such, a full understanding of the biology of the LHR is essential to the survival of our species. In this review we summarize our current knowledge of the structure, functions, and regulation of this important receptor.
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                Author and article information

                Contributors
                hrskishi@gmail.com
                Journal
                Reprod Med Biol
                Reprod. Med. Biol
                10.1111/(ISSN)1447-0578
                RMB2
                Reproductive Medicine and Biology
                John Wiley and Sons Inc. (Hoboken )
                1445-5781
                1447-0578
                07 December 2017
                January 2018
                : 17
                : 1 ( doiID: 10.1111/rmb2.2018.17.issue-1 )
                : 11-19
                Affiliations
                [ 1 ] Department of Obstetrics and Gynecology Gunma University Hospital Gunma Japan
                Author notes
                [*] [* ] Correspondence

                Hiroshi Kishi, Department of Obstetrics and Gynecology, Gunma University Hospital, Gunma, Japan.

                Email: hrskishi@ 123456gmail.com

                Author information
                http://orcid.org/0000-0003-1562-410X
                Article
                RMB212075
                10.1002/rmb2.12075
                5768975
                29371816
                89fde1b4-0965-493c-8c8f-224ba950c55d
                © 2017 The Authors. Reproductive Medicine and Biology published by John Wiley & Sons Australia, Ltd on behalf of Japan Society for Reproductive Medicine.

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 31 July 2017
                : 26 October 2017
                Page count
                Figures: 3, Tables: 0, Pages: 11, Words: 5805
                Categories
                Review Article
                Review Articles
                Custom metadata
                2.0
                rmb212075
                January 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.2.8 mode:remove_FC converted:16.01.2018

                follicle‐stimulating hormone receptor,granulosa cells,luteinizing hormone receptor,receptor downregulation,theca cells

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