Effect of anti-mullerian hormone in hypothalamic Kiss-1- and GnRH-producing cell models
Effect of anti-mullerian hormone in hypothalamic Kiss-1- and GnRH-producing cell models
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抗苗勒氏管激素对下丘脑 Kiss-1 和 GnRH 产生细胞模型的影响
DOI：
10.1080/09513590.2021.1950134
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发表时间：
2021
影响因子：
2
通讯作者：
Kyo S.
中科院分区：
文献类型：
--
作者：
Oride A;Kanasaki H;Tumurbaatar T;Tumurgan Z;Okada H;Kyo S.
目的：抗苗勒管激素（AMH）是参与卵泡发育的局部因子之一。此外，AMH及其受体在全身广泛表达。材料和方法：mHypoA-50和mHypoA-55细胞分别来源于下丘脑前腹侧室周核（anteroventricular periventricular nucleus，AVPV）和弓状核（arctic nucleus，ARC），这些细胞被称为Kiss-1（编码kisspeptin）表达细胞模型。这些细胞还表达促性腺激素释放激素（GnRH）基因。结果：mHypoA-50和mHypoA-55下丘脑细胞均表达AMH和AMH受体2（AMHR 2）。外源性AMH未能改变两种细胞模型中Kiss-1基因的表达水平，但在mHypoA-50 AVPV细胞中，100 pM时GnRH基因表达显著增加1.73 ± 0.2倍，在mHypoA-55 ARC细胞中，1 nM时GnRH基因表达显著增加1.74 ± 0.17倍。AMH也增加了两种细胞模型中GnRH蛋白的表达。与下丘脑细胞系中观察到的现象相似，100 pM AMH显著增加了胎鼠脑细胞原代培养物中GnRH，但不增加Kiss-1 mRNA的表达。Kisspeptin-10（KP 10）可增加mHypoA-55 ARC细胞中Kiss-1基因的表达，但这一作用被AMH阻断。AMH不影响mHypoA-55 ARC细胞Kissspeptin受体（Kiss 1 R）、神经激肽B和强啡肽A的表达。此外，AMH可能是KP 10诱导的Kiss-1基因表达的有效抑制剂。
Purpose:Anti-Müllerian hormone (AMH) is one of the local factors involved in follicle development. In addition, AMH and its receptor are broadly expressed throughout the body. In this study, we examined how AMH modifies gene expression of Kiss-1 and GnRH.Materials and methods:mHypoA-50 and mHypoA-55 cells were originated from the hypothalamic anteroventral periventricular nucleus (AVPV) and arcuate nucleus (ARC), respectively, and these cells are known as Kiss-1 (which encodes kisspeptin) expressing cell models. These cells also express gonadotropin-releasing hormone (GnRH) genes. Our experiments were performed useing these cell models.Results:Both mHypoA-50 and mHypoA-55 hypothalamic cells expressed AMH and AMH receptor type 2 (AMHR2). Exogenous AMH failed to alter the expression levels of the Kiss-1 gene in both cell models but significantly increased GnRH gene expression by 1.73 ± 0.2-fold at 100 pM in mHypoA-50 AVPV cells and by 1.74 ± 0.17-fold at 1 nM in mHypoA-55 ARC cells. AMH also augmented GnRH protein expression in both cell models. Similar to the phenomenon observed in the hypothalamic cell lines, 100 pM AMH significantly increased GnRH, but not Kiss-1, mRNA expression in primary cultures of fetal rat brain cells. Kisspeptin-10 (KP10) increased Kiss-1 gene expression in mHypoA-55 ARC cells but this was blocked by AMH. AMH did not alter the expression of the kisspeptin receptor (Kiss1R) or that of neurokinin B or dynorphin A in mHypoA-55 ARC cells.Conclusions:It was demonstrated that AMH participates in hypothalamic-pituitary-gonadal axis control by stimulating GnRH expression. In addition, AMH might be a potent repressor of Kiss-1 gene expression induced by KP10.