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The G protein-coupled estrogen receptor (GPER) was proved to be a new type of estrogen receptor (ER). It is unknown that whether estrogen can regulate the secretion of gonadotrophin releasing hormone (GnRH) in GT1-7 cells through the mechanism with the involvement of GPER. The GnRH, estradiol (17β-estradiol, E2) and GPER in peripheral blood of precocious puberty children were detected by ELISA and RT-qPCR assays. After E2 treatment, the levels of GPER and GnRH in GT1-7 cells were detected. Following G1 treatment, cell proliferation was examined using a CCK-8 assay. The levels of GnRH, KISS1, GPR54, nNOS, c-FOS in GT1-7 cells were assessed following GT1-7 cells were induced by E2 combined with G1 or G15. GnRH, E2 and GPER were significantly increased in precocious puberty children. After E2 treatment, GT1-7 cells expressed more GnRH and GPER was markedly elevated and reached a peak at 8 h. The KISS1, GPR54 and nNOS in GT1-7 cells were significantly increased with G1 induction, but were significantly decreased with G15 induction compared with E2 induction alone. Collectively, GPER cannot promote the release of GnRH via affecting the proliferation of GT1-7 cells, but it may regulate GnRH through KISS1/GPR54 pathway, which provides novel ideas for precocious puberty children treatment.

general physiology and biophysics

Estrogen can promote the expression of genes related to precocious puberty in GT1-7 mouse hypothalamic GnRH neuronal cell line via activating G protein-coupled estrogen receptor