BACKGROUND The interstitium of the mouse testis contains Leydig cells and a small number of steroidogenic cells with adrenal characteristics which may be derived from the fetal adrenal during development or may be a normal subset of the developing fetal Leydig cells. Currently it is not known what regulates development and/or proliferation of this sub-population of steroidogenic cells in the mouse testis. Androgen receptors (AR) are essential for normal testicular function and in this study we have examined the role of the AR in regulating interstitial cell development. RESULTS Using a mouse model which lacks gonadotropins and AR (hpg.ARKO), stimulation of luteinising hormone receptors in vivo with human chorionic gonadotropin (hCG) caused a marked increase in adrenal cell transcripts/protein in a group of testicular interstitial cells. hCG also induced testicular transcripts associated with basic steroidogenic function in these mice but had no effect on adult Leydig cell-specific transcript levels. In hpg mice with functional AR, treatment with hCG induced Leydig cell-specific function and had no effect on adrenal transcript levels. Examination of mice with cell-specific AR deletion and knockdown of AR in a mouse Leydig cell line suggests that AR in the Leydig cells are likely to regulate these effects. CONCLUSIONS This study shows that in the mouse the androgen receptor is required both to prevent development of testicular cells with adrenal characteristics and to ensure development of an adult Leydig cell phenotype.

中文翻译：

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需要雄激素受体表达来确保成年Leydig细胞的发育并防止小鼠睾丸中具有肾上腺特征的类固醇生成细胞的发育。

背景技术小鼠睾丸的间质中含有莱迪奇细胞和少量具有肾上腺特性的类固醇生成细胞，它们可能是在发育过程中从胎儿肾上腺衍生的，或者是发育中的胎儿莱迪奇细胞的正常子集。目前尚不清楚什么调节小鼠睾丸中类固醇生成细胞亚群的发育和/或增殖。雄激素受体（AR）对于正常的睾丸功能至关重要，在这项研究中，我们研究了AR在调节间质细胞发育中的作用。结果使用缺乏促性腺激素和AR（hpg.ARKO）的小鼠模型，人绒毛膜促性腺激素（hCG）在体内刺激黄体生成激素受体会导致一组睾丸间质细胞的肾上腺细胞转录物/蛋白质显着增加。在这些小鼠中，hCG还诱导了与基本类固醇生成功能相关的睾丸转录本，但对成年Leydig细胞特异性转录本水平没有影响。在具有功能性AR的hpg小鼠中，用hCG处理可诱导Leydig细胞特异性功能，并且对肾上腺转录水平没有影响。对小鼠的细胞特异性AR缺失和小鼠Leydig细胞系中的AR敲低的检查表明，Leydig细胞中的AR可能调节这些作用。结论这项研究表明，在小鼠中需要雄激素受体来防止具有肾上腺特征的睾丸细胞的发育并确保成年Leydig细胞表型的发育。在具有功能性AR的hpg小鼠中，用hCG处理可诱导Leydig细胞特异性功能，并且对肾上腺转录水平没有影响。对小鼠的细胞特异性AR缺失和小鼠Leydig细胞系中的AR敲低的检查表明，Leydig细胞中的AR可能调节了这些作用。结论这项研究表明，在小鼠中需要雄激素受体来防止具有肾上腺特征的睾丸细胞的发育并确保成年Leydig细胞表型的发育。在具有功能性AR的hpg小鼠中，用hCG处理可诱导Leydig细胞特异性功能，并且对肾上腺转录水平没有影响。小鼠Leydig细胞系中具有细胞特异性AR缺失和AR敲低的小鼠研究表明，Leydig细胞中的AR可能调节了这些作用。结论这项研究表明，在小鼠中需要雄激素受体来防止具有肾上腺特征的睾丸细胞的发育并确保成年Leydig细胞表型的发育。