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学科主题: 临床医学
题名:
Infertility with defective spermatogenesis and steroidogenesis in male mice lacking androgen receptor in Leydig cells
作者: Xu, Qingquan; Lin, Hung-Yun; Yeh, Shauh-Der; Yu, I-Chen; Wang, Ruey-Shen; Chen, Yen-Ta; Zhang, Caixia; Altuwaijri, Saleh; Chen, Lu-Min; Chuang, Kuang-Hsiang; Chiang, Han-Sun; Yeh, Shuyuan; Chang, Chawnshang
关键词: androgen receptor ; leydig cell ; steroidogenesis ; spermatogenesis
刊名: ENDOCRINE
发表日期: 2007-08-01
DOI: 10.1007/s12020-007-9015-0
卷: 32, 期:1, 页:96-106
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Endocrinology & Metabolism
研究领域[WOS]: Endocrinology & Metabolism
关键词[WOS]: ADULT-RAT ; POSTNATAL-DEVELOPMENT ; SERTOLI-CELLS ; NEONATAL-HYPOTHYROIDISM ; EXPERIMENTAL-ANIMALS ; IN-VITRO ; MOUSE ; TESTOSTERONE ; DIFFERENTIATION ; KNOCKOUT
英文摘要:

Androgen and the androgen receptor (AR) have been shown to play critical roles in male fertility. Our previous data demonstrated that mice lacking AR (AR(-/y)) revealed incomplete germ cell development and lowered serum testosterone levels, which resulted in azoospermia and infertility. However, the consequences of AR loss in Leydig cells remain largely unknown. Using a Cre-LoxP conditional knockout strategy, we generated a tissue-specific knockout mouse (L-AR(-/y)) with the AR gene deleted by the anti-Mullerian hormone receptor-2 (Amhr2) promoter driven Cre expressed in Leydig cells. Phenotype analyses show that the outside appearance of L-AR(-/y) mice was indistinguishable from wild type mice (AR(+/y)), but with atrophied testes and epididymis. L-AR(-/y) mice were infertile, with spermatogenic arrest predominately at the round spermatid stage and no sperm could be detected in the epididymis. L-AR(-/y) mice also have lower serum testosterone concentrations and higher serum leuteinizing hormone and follicle-stimulating hormone concentrations than AR(+/y) mice. Further mechanistic studies demonstrated that hypotestosteronemia in L-AR(-/y) mice is not caused by reducing numbers of Leydig cells, but instead by the alterations of several key steroidogenic enzymes, including 17 beta-HSD3, 3 beta-HSD6, and P450c17. Together, L-AR(-/y) mice provide in vivo evidence that functional AR in Leydig cells is essential to maintain normal spermatogenesis, testosterone production, and required for normal male fertility.

语种: 英语
WOS记录号: WOS:000250834600012
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/65265
Appears in Collections:北京大学第二临床医学院_泌尿外科_期刊论文

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作者单位: 1.Univ Rochester, Dept Urol, Ctr Canc, Rochester, NY 14642 USA
2.Taipei Med Univ, Grad Inst Med Sci, Taipei 110, Taiwan
3.Taipei Med Univ, Dept Urol, Taipei 110, Taiwan
4.Univ Rochester, Dept Pathol, Ctr Canc, Rochester, NY 14642 USA
5.Univ Rochester, George Whipple Lab Canc Res, Rochester, NY 14642 USA
6.Peking Univ, Peoples Hosp, Dept Urol, Beijing 100871, Peoples R China
7.Taipei Med Univ, Dept Gynecol & Obstet, Taipei 110, Taiwan
8.Fu Jen Catholic Univ Coll Med, Taipei, Taiwan

Recommended Citation:
Xu, Qingquan,Lin, Hung-Yun,Yeh, Shauh-Der,et al. Infertility with defective spermatogenesis and steroidogenesis in male mice lacking androgen receptor in Leydig cells[J]. ENDOCRINE,2007,32(1):96-106.
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