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雌激素可通过激活G蛋白偶联雌激素受体,促进GT1-7小鼠下丘脑促性腺激素释放激素(GnRH)神经元细胞系中与性早熟相关基因的表达。

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.

作者信息

Qian Fang, Shi Nian, Zhou Huan

机构信息

Department of Eugenics and Genetics, Family Planning Science and Technology Institute, Xinxiang Uygur Autonomous Region, Urumqi, China.

出版信息

Gen Physiol Biophys. 2020 Jan;39(1):27-36. doi: 10.4149/gpb_2019049.

Abstract

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.

摘要

G蛋白偶联雌激素受体(GPER)被证明是一种新型雌激素受体(ER)。雌激素是否能通过涉及GPER的机制调节GT1-7细胞中促性腺激素释放激素(GnRH)的分泌尚不清楚。采用ELISA和RT-qPCR检测性早熟儿童外周血中的GnRH、雌二醇(17β-雌二醇,E2)和GPER。E2处理后,检测GT1-7细胞中GPER和GnRH的水平。G1处理后,采用CCK-8法检测细胞增殖。用E2联合G1或G15诱导GT1-7细胞后,评估GT1-7细胞中GnRH、KISS1、GPR54、nNOS、c-FOS的水平。性早熟儿童的GnRH、E2和GPER显著升高。E2处理后,GT1-7细胞表达更多的GnRH,GPER明显升高,并在8小时达到峰值。与单独E2诱导相比,G1诱导GT1-7细胞中的KISS1、GPR54和nNOS显著增加,但G15诱导则显著降低。总的来说,GPER不能通过影响GT1-7细胞的增殖来促进GnRH的释放,但它可能通过KISS1/GPR54途径调节GnRH,这为性早熟儿童的治疗提供了新的思路。

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