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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Oligozoospermia with normal fertility in male mice lacking the androgen receptor in testis peritubular myoid cells
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Oligozoospermia with normal fertility in male mice lacking the androgen receptor in testis peritubular myoid cells

机译：雄性睾丸小管周围肌细胞缺乏雄激素受体的雄性小鼠少精症

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摘要

Androgens and the androgen receptor (AR) play important roles in the testes. Previously we have shown that male total AR knockout (T-AR(-/y)) mice revealed incomplete germ cell development and lowered serum testosterone levels, which resulted in azoospermia and infertility. However, the consequences of AR loss in particular types of testicular cells remain unclear. Using a Cre-loxP conditional knockout strategy, we generated a tissue-selective knockout mouse with the AR gene deleted in testis peritubular myoid cells (PM-AR(-/y)). Phenotype analyses showed that PM-AR(-/y) mice were indistinguishable from WT AR (AR(+/y)) mice with the exception of smaller testes size. PM-AR(-/y) mice have serum testosterone concentrations comparable with AR(+/y) mice. PM-AR(-/y) mice have oligozoospermia in the epididymis; however, fertility was normal. Although normal germ cell distribution ratio was found, total germ cell number decreased in PM-AR(-/y) mice. Further mechanistic studies demonstrated that PM-AR(-/y) mice have defects in the expression of Sertoli cells' functional marker genes such as tran-ferrin, epidermal fatty acid-binding protein, androgen-binding protein, and other junction genes including occludin, testin, nectin, zyxin, vinculin, laminin gamma 3, gelsolin, connection43, and N-cadherin. Furthermore, there were defects in peritubular myoid cell contractility-related genes such as endothelin-1, endothelin receptor A and B, adrenomedullin, adrenomedullin receptor, and vasopressin receptor 1 a. Together, our PM-AR(-/y) mice provide in vivo evidence for the requirement of functional AR in peritubular myoid cells to maintain normal Sertoli cells function and peritubular myoid cell contractility, thus ensuring normal spermatogenesis and sperm output.
机译：雄激素和雄激素受体（AR）在睾丸中起重要作用。以前我们已经表明，雄性总AR基因敲除（T-AR（-/ y））小鼠显示生殖细胞发育不完全和血清睾丸激素水平降低，从而导致无精子症和不育症。然而，AR丢失在特定类型的睾丸细胞中的后果仍不清楚。使用Cre-loxP条件敲除策略，我们生成了一个组织选择性敲除小鼠，其AR基因在睾丸肾小管周围肌样细胞（PM-AR（-/ y））中缺失。表型分析表明，除睾丸较小外，PM-AR（-/ y）小鼠与WT AR（AR（+ / y））小鼠没有区别。 PM-AR（-/ y）小鼠的血清睾丸激素浓度与AR（+ / y）小鼠相当。 PM-AR（-/ y）小鼠的附睾有少精症。但是，生育能力是正常的。尽管发现正常的生殖细胞分布比率，但PM-AR（-/ y）小鼠的总生殖细胞数量减少。进一步的机理研究表明，PM-AR（-/ y）小鼠在支持细胞功能标记基因（如转铁蛋白，表皮脂肪酸结合蛋白，雄激素结合蛋白）以及其他连接基因（包括闭合蛋白）的表达中存在缺陷，testin，nectin，zyxin，vincinin，层粘连蛋白gamma 3，凝溶胶蛋白，connection43和N-cadherin。此外，在肾小管周围肌细胞收缩性相关基因如内皮素-1，内皮素受体A和B，肾上腺髓质素，肾上腺髓质素受体和血管加压素受体1a中存在缺陷。我们的PM-AR（-/ y）小鼠在一起提供了体内证据，证明肾小管周肌细胞中功能性AR需要维持正常的Sertoli细胞功能和肾小管周肌细胞收缩性，从而确保正常的精子发生和精子输出。

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