IMR Press / FBE / Volume 2 / Issue 4 / DOI: 10.2741/E181

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Signal pathway of GnRH-III inhibiting FSH-induced steroidogenesis in granulosa cells
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1 State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, No. 5 Datun Road, Chaoyang District, Beijing 100101, China
2 Graduate School of the Chinese Academy of Sciences, Beijing 100039, China
3 School of Life Science and Technology, Beijing Institute of Technology, Beijing 10001, China
Academic Editor:Xinchang Zhou
Front. Biosci. (Elite Ed) 2010, 2(4), 1218–1226;
Published: 1 June 2010
(This article belongs to the Special Issue Reproductive biology)

Gonadotrophin-releasing hormone type 1 and type 2 have been demonstrated to inhibit follicle-stimulating hormone (FSH)-induced granulosa cell (GC) steroidogenesis. A third type of GnRH (GnRH-III) was also purified from salmon, its action on the FSH-regulated GC function, however is not clear. In the present study we demonstrated that the FSH-induced estrogen and progesterone production in cultured DES-treated GCs was significantly inhibited by GnRH-III. Furthermore, the FSH-stimulated steroidogenic acute regulatory protein and the enzymes for steroidigenesis, such as HSD3B2,aromatase and cytochrome P450 side-chain cleavage were also significantly suppressed by this peptide. The inhibitory action of GnRH-III on the FSH-induced steroidogenenisis was demonstrated via Akt and p38 mitogen-activated protein kinase signaling pathways through suppressing its own receptor expression. Further studies indicated that FSH could stimulate NR5A2 and upstream stimulatory factor (USF) activation, and their induction was significantly suppressed by the GnRH-III. Therefore, it is suggested that GnRH-III inhibiting FSH-induced steroidogenenisis in GCs might be by suppressing FSH-induced its own receptor expression via NR5A2 and USF transcriptional factors.

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