Localization of gonadotropin-releasing hormone (GnRH), gonadotropin-inhibitory hormone (GnIH), kisspeptin and GnRH receptor and their possible roles in testicular activities from birth to senescence in mice.

Localization of gonadotropin-releasing hormone (GnRH), gonadotropin-inhibitory hormone (GnIH), kisspeptin and GnRH receptor and their possible roles in testicular activities from birth to senescence in mice.
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DOI:
10.1002/jez.1765
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发表时间:
2012-12
影响因子:
2.8
通讯作者:
Tsutsui, Kazuyoshi
Tsutsui, Kazuyoshi
中科院分区:
生物学3区
文献类型:
--
作者:
Anjum, Shabana;Krishna, Amitabh;Sridaran, Rajagopala;Tsutsui, Kazuyoshi

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观察了小鼠从出生到衰老过程中神经肽、促性腺激素释放激素(GnRH)、促性腺激素抑制激素(GnIH)、促性腺激素释放激素受体(GnRH-R)、促性腺激素释放激素释放激素(GnRH)、促性腺激素释放激素释放激素(GnRH)、促性腺激素释放激素释放激素(GnRH)、细胞色素P450侧链裂解酶(P450 SCC)活性、睾丸雄激素受体(AR)和血清睾酮水平等生殖参数的变化。结果表明,这些分子主要分布在间质细胞和生殖细胞中,并且从出生到衰老免疫抑制作用有明显的变化。结果发现,在青春期和成年期,睾丸GnRH-R表达的增强与类固醇合成活性的增强相一致,而在衰老阶段,睾丸GnRH-R的表达减弱与类固醇合成活性的降低相一致。免疫印迹分析也证实了类似的免疫染色变化。因此,这些结果提示GnRH可能在睾丸青春期发育和衰老过程中起作用。用GnRH激动剂([DTrp6,Pro9-net]GnRH)处理小鼠从青春期前到青春期的小鼠睾丸类固醇合成活性显著增加,进一步支持了GnRH在睾丸青春期成熟中的作用。GnRH-R在衰老过程中的显著下降可能是由于衰老过程中GnIH合成显著增加,导致GnRH-R表达下降所致。GnRH-R水平的显著变化可能是导致小鼠睾丸青春期激活或衰老的类固醇激素合成变化的原因。此外,GnRH-R水平的变化可能受GnRH、GnIH和Kispeptin在睾丸中的相互作用的调节。
The changes in distribution and concentration of neuropeptides, gonadotropin-releasing hormone (GnRH), gonadotropin-inhibitory hormone (GnIH), kisspeptin, and gonadotropin-releasing hormone receptor (GnRH-R) were evaluated and compared with reproductive parameters, such as cytochrome P450 side-chain cleavage (P450 SCC) enzyme activity, androgen receptors (AR) in the testis and serum testosterone levels, from birth to senescence in mice. The results showed the localization of these molecules mainly in the interstitial and germ cells as well as showed significant variations in immunostatining from birth to senescence. It was found that increased staining of testicular GnRH-R coincided with increased steroidogenic activity during pubertal and adult stages, whereas decreased staining coincides with decreased steroidogenic activity during senescence. Similar changes in immunostaining were confirmed by Western/slot blot analysis. Thus, these results suggest a putative role of GnRH during testicular pubertal development and senescence. Treatment with a GnRH agonist ([DTrp6, Pro9-NEt] GnRH) to mice from prepubertal to pubertal period showed a significant increase in steroidogenic activity of the mouse testis and provided further support to the role of GnRH in testicular pubertal maturation. The significant decline in GnRH-R during senescence may be due to a significant increase in GnIH synthesis during senescence causing the decrease in GnRH-R expression. It is considered that significant changes in the levels of GnRH-R may be responsible for changes in steroidogenesis that causes either pubertal activation or senescence in testis of mice. Furthermore, changes in the levels of GnRH-R may be modulated by interactions among GnRH, GnIH, and kisspeptin in the testis.
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