OBJECTIVES:Sex steroid hormones play roles in the regulation of pituitary hormone synthesis and secretion. Here we investigated the role of estradiol (E2) and progesterone (P4) on pituitary gonadotropin luteinizing hormone (LH)β- and follicle stimulating hormone (FSH)β-transcriptional activity in a single colony of gonadotroph LβT2 cells. METHODS:Pituitary gonadotroph cell line, LβT2 cells were used in this study. Cells were transfected with LHβ- or FSHβ-subunit promoter region-linked luciferase vector, and stimulated with gonadotropin-releasing hormone (GnRH) in the presence or absence of sex steroids. Transcriptional activity for LHβ- and FSHβ-subunit were determined by luciferase assay. Effects of sex steroids on cell proliferation was also determined by measurement of 5-bromoe-2'-deoxyuridine (BrdU) incorporation. RESULTS:The basal promoter activity of the LHβ subunit was not modulated by 10 nM E2, but gonadotropin releasing hormone (GnRH)-induced LHβ promoter activity was significantly increased by the same concentration of E2. Similarly, although the basal FSHβ promoter was not modulated by 10 nM E2, GnRH-induced FSHβ promoters were significantly potentiated in the presence of E2. One micromole E2 modulated neither basal nor GnRH-induced LHβ and FSHβ promoters. On the other hand, basal LHβ promoter activity was enhanced by 1 µM P4, but the stimulatory response of GnRH on LHβ promoters was significantly inhibited in the presence of 1 µM P4. Similar to LHβ promoters, the basal activity of the FSHβ promoter was increased by 1 µM P4; however, the response to GnRH was not modulated in the presence of P4. Ten micromoles P4 modified neither basal nor GnRH-induced promoter activity for LHβ and FSHβ. E2 had no antagonistic effect on P4-induced basal promoter activities of LHβ or FSHβ. A cell proliferation assay showed that neither E2 nor P4 modulated the growth of LβT2 cells, even in the presence or absence of GnRH. CONCLUSION:These observations suggest that both E2 and P4 uniquely modulate basal and GnRH-stimulated gonadotropin promoters without affecting cell growth.

译文

目的:性类固醇激素在垂体激素合成和分泌的调节中发挥作用。在这里,我们研究了雌二醇(E2)和孕酮(P4)在促性腺激素LβT2细胞单个菌落中对垂体促性腺激素促黄体生成激素(LH)β-和促卵泡激素(FSH)β-转录活性的作用。
方法:采用垂体促性腺激素细胞系LβT2。用LHβ-或FSHβ-亚基启动子区域连接的荧光素酶载体转染细胞,并在存在或不存在性类固醇的情况下用促性腺激素释放激素(GnRH)刺激细胞。通过荧光素酶测定法测定LHβ-和FSHβ-亚基的转录活性。性类固醇对细胞增殖的影响还可以通过测量5-溴2'-脱氧尿苷(BrdU)的掺入来确定。
结果:10 nM E2不能调节LHβ亚基的基础启动子活性,但是在相同浓度的E2下,促性腺激素释放激素(GnRH)诱导的LHβ启动子活性显着增加。类似地,尽管基础FSHβ启动子不受10 nM E2调节,但在E2存在下,GnRH诱导的FSHβ启动子显着增强。一微摩尔E2既不调节基础也不刺激GnRH诱导的LHβ和FSHβ启动子。另一方面,基础LHβ启动子活性被1μMP4增强,但是在1μMP4存在下,GnRH对LHβ启动子的刺激反应被显着抑制。与LHβ启动子相似,FSHβ启动子的基础活性增加1 µM P4。然而,在P4存在下,对GnRH的反应没有被调节。十微摩尔P4既不改变基础也不改变GnRH诱导的LHβ和FSHβ启动子活性。 E2对P4诱导的LHβ或FSHβ的基础启动子活性没有拮抗作用。细胞增殖试验表明,即使存在或不存在GnRH,E2和P4均不能调节LβT2细胞的生长。
结论:这些观察结果表明,E2和P4均可唯一调节基础和GnRH刺激的促性腺激素启动子,而不会影响细胞生长。

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