Roles of Intracerebral Activin, Inhibin, and Follistatin in the Regulation of Kiss-1 Gene Expression: Studies Using Primary Cultures of Fetal Rat Neuronal Cells.

Roles of Intracerebral Activin, Inhibin, and Follistatin in the Regulation of Kiss-1 Gene Expression: Studies Using Primary Cultures of Fetal Rat Neuronal Cells.
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脑内激活素、抑制素和卵泡抑素在 Kiss-1 基因表达调节中的作用:使用胎鼠神经元细胞原代培养物的研究。

DOI:
10.1016/j.bbrep.2020.100785
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发表时间:
2020
影响因子:
2.7
通讯作者:
Okada H and Kyo S
Okada H and Kyo S
中科院分区:
--
文献类型:
--
作者:
90.Tumurgan Z;Kanasaki H;Tumurbaatar T;Oride A;Okada H and Kyo S

文献摘要

相似文献

由Kiss-1基因编码的下丘脑kisspeptin通过直接调节促性腺激素释放激素的释放来支配下丘脑-垂体-性腺轴。在这项研究中,我们研究的作用,激活素,kisspeptin,和卵泡抑素的调节Kiss-1基因的表达,使用原代培养的胎鼠神经元细胞,表达Kiss-1基因和kisspeptin。用激活素刺激使这些培养物中Kiss-1基因表达显著增加2.02 ± 0.39倍。与此相反,Kiss-1基因表达的显着减少,观察到与阿托伐他汀A和卵泡抑素治疗。抑制素B不调节Kiss-1基因表达。激活素、卵泡抑素和卵泡抑素也在胎鼠脑培养物中表达,它们的表达受雌二醇(E2)控制。E2可上调α、βA和βB亚基的表达。同样,卵泡抑素基因表达显着增加E2在这些细胞。我们的研究结果表明,激活素的可能性,E2诱导的反馈控制的下丘脑-垂体-性腺轴的脑中表达的follistatin,follistatin和follistatin。
Hypothalamic kisspeptin, encoded by the Kiss-1 gene, governs the hypothalamic-pituitary-gonadal axis by directly regulating the release of gonadotropin-releasing hormone. In this study, we examined the roles of activin, inhibin, and follistatin in the regulation of Kiss-1 gene expression using primary cultures of fetal rat neuronal cells, which express the Kiss-1 gene and kisspeptin. Stimulation with activin significantly increased Kiss-1 gene expression in these cultures by 2.02 ± 0.39-fold. In contrast, a significant decrease in Kiss-1 gene expression was observed with inhibin A and follistatin treatment. Inhibin B did not modulate Kiss-1 gene expression. Activin, inhibin, and follistatin were also expressed in fetal rat brain cultures and their expression was controlled by estradiol (E2). The inhibin α, βA, and βB subunits were upregulated by E2. Similarly, follistatin gene expression was significantly increased by E2 in these cells. Our results suggest the possibility that activin, inhibin, and follistatin expressed in the brain participate in the E2-induced feedback control of the hypothalamic-pituitary-gonadal axis.