G protein-coupled estrogen receptor 1 (GPER 1) mediates estrogen-induced, proliferation of leiomyoma cells
G protein-coupled estrogen receptor 1 (GPER 1) mediates estrogen-induced, proliferation of leiomyoma cells
复制标题
G 蛋白偶联雌激素受体 1 (GPER 1) 介导雌激素诱导的平滑肌瘤细胞增殖
DOI：
10.3109/09513590.2015.1092022
复制
发表时间：
2015-09
影响因子：
2
通讯作者：
Lin J
中科院分区：
文献类型：
--
作者：
Ma J;Li W;Wu RJ;Lin J
Abstract G protein-coupled estrogen receptor 1 (GPER-1, formerly known as GPR30) has been proposed as the receptor for estrogen-induced, growth of leiomyomas though its precise mechanisms of action are not clear. We obtained leiomyoma cells (LC) and normal smooth muscle cells from 28 women (n = 28, median age 38 years, median parity 1.0). We incubated them with 17-β estradiol (E2), after blocking, or upregulating, expression of GPER-1 with ICI182,780 (a GPER-1 agonist) and siGPR30, respectively. We evaluated the role of GPER-1 in the mitogen-activated protein kinase (MAPK) signaling pathway using Western blot analysis. We studied cell proliferation with 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide, and, mitotic activity with phosphohistone H3 (PPH3) expression in leiomyoma, and, matched, normal, smooth muscle tissues using standard immunohistochemistry. Downregulation of GPER-1 expression with siGPR30 partially attenuated the E2-activated MAPK signaling pathway (p < 0.01). Upregulation of GPER-1 with ICI182,780 enhanced the E2-activated MAPK signaling pathway (p < 0.01). ICI182,780 enhanced E2-induced proliferation of LC (p < 0.01), while knock down of the GPER-1 gene with GPER-1 small interfering RNA partially inhibited E2-induced cell proliferation (p < 0.01). There were no significant differences in PPH3 expression between LCs and normal smooth muscle tissues (p > 0.05). Neither ICI182,780 nor siGPR30 increased mitosis in LCs (p > 0.05). Our results indicate that GPER-1 mediates proliferation of estrogen-induced, LC by activating the MAPK pathway, and, not by promoting mitosis. Chinese abstract G蛋白偶联雌激素受体1(GPER-1, 曾用名GPR30)被认为是雌激素导致平滑肌瘤细胞(LC)增殖的受体，即使具体的机制并未明确。我们从28名妇女（n=28，年龄中值 38 岁，奇偶校验中值1.0）体内获取了平滑肌瘤细胞（LC）和正常平滑肌细胞。分别使用ICI182,780 (一种GPER-1兴奋剂)和 siGPR30抑制或上调GPER-1表达后17-β雌激素 (E2)孵育细胞。使用Western blot分析GPER-1在丝裂原活化蛋白激酶(MAPK)信号通路中的作用。平滑肌细胞增殖情况和分裂活性分别使用噻唑蓝和组蛋白H3 (PPH3)的表达水平观察，与之对应的正常平滑肌细胞作标准免疫组织化学染色。siGPR30下调GPER-1表达可部分抑制E2活化的MAPK信号通路(p<0.01)。 ICI182,780上调GPER-1表达后E2活化的MAPK信号通路增强(p<0.01)。 ICI182,780可提高E2导致的LC增殖(p<0.01)，GPER-1小干扰RNA敲除GPER-1基因部分抑制E2所致细胞增殖(p<0.01)。LC细胞与正常平滑肌细胞的PPH3表达水平并没有显著差异(p>0.05)。 ICI182,780和siGPR30均不能造成LCs增殖(p>0.05)。我们的结果表明GPER-1通过活化MAPK通路调节雌激素导致的LC增殖，而非促进有丝分裂。
登录
查看更多内容
影响因子：
7.4
作者：
Rettberg, Jamaica R.;Yao, Jia;Brinton, Roberta Diaz
通讯作者：
Brinton, Roberta Diaz
与 aquaporin-5 下调相关的 Ishikawa 细胞迁移减少
影响因子：
2.9
作者：
Jiang, Xiu Xiu;Xu, Kai Hong;Wu, Rui Jin
通讯作者：
Wu, Rui Jin
影响因子：
--
作者：
E. Filardo;Jeffrey A. Quinn;K. Bland;A. Frackelton;Roger Williams
通讯作者：
E. Filardo;Jeffrey A. Quinn;K. Bland;A. Frackelton;Roger Williams
DOI：
10.1006/bbrc.1996.1654
发表时间：
1996-11-12
影响因子：
3.1
作者：
Owman, C;Blay, P;Lolait, SJ
通讯作者：
Lolait, SJ
影响因子：
1.8
作者：
Fung, Adele D.;Cohen, Cynthia;Reid, Michelle D.
通讯作者：
Reid, Michelle D.