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缺乏促卵泡激素和雄激素的支持细胞受体的小鼠的精子发生和支持细胞活性

Spermatogenesis and sertoli cell activity in mice lacking sertoli cell receptors for follicle-stimulating hormone and androgen.

作者信息

Abel M H, Baker P J, Charlton H M, Monteiro A, Verhoeven G, De Gendt K, Guillou F, O'Shaughnessy P J

机构信息

Department of Human Anatomy and Genetics, University of Oxford, Oxford, UK.

出版信息

Endocrinology. 2008 Jul;149(7):3279-85. doi: 10.1210/en.2008-0086. Epub 2008 Apr 10.

Abstract

Spermatogenesis in the adult male depends on the action of FSH and androgen. Ablation of either hormone has deleterious effects on Sertoli cell function and the progression of germ cells through spermatogenesis. In this study we generated mice lacking both FSH receptors (FSHRKO) and androgen receptors on the Sertoli cell (SCARKO) to examine how FSH and androgen combine to regulate Sertoli cell function and spermatogenesis. Sertoli cell number in FSHRKO-SCARKO mice was reduced by about 50% but was not significantly different from FSHRKO mice. In contrast, total germ cell number in FSHRKO-SCARKO mice was reduced to 2% of control mice (and 20% of SCARKO mice) due to a failure to progress beyond early meiosis. Measurement of Sertoli cell-specific transcript levels showed that about a third were independent of hormonal action on the Sertoli cell, whereas others were predominantly androgen dependent or showed redundant control by FSH and androgen. Results show that FSH and androgen act through redundant, additive, and synergistic regulation of spermatogenesis and Sertoli cell activity. In addition, the Sertoli cell retains a significant capacity for activity, which is independent of direct hormonal regulation.

摘要

成年雄性的精子发生依赖于促卵泡激素(FSH)和雄激素的作用。去除任何一种激素都会对支持细胞功能以及生殖细胞通过精子发生过程的进展产生有害影响。在本研究中,我们构建了同时缺乏FSH受体(FSHRKO)和支持细胞上雄激素受体(SCARKO)的小鼠,以研究FSH和雄激素如何共同调节支持细胞功能和精子发生。FSHRKO - SCARKO小鼠的支持细胞数量减少了约50%,但与FSHRKO小鼠没有显著差异。相比之下,FSHRKO - SCARKO小鼠的生殖细胞总数减少到对照小鼠的2%(以及SCARKO小鼠的20%),原因是无法超越减数分裂早期阶段。对支持细胞特异性转录水平的测量表明,约三分之一的转录水平独立于激素对支持细胞的作用,而其他转录水平主要依赖雄激素,或显示出FSH和雄激素的冗余调控。结果表明,FSH和雄激素通过对精子发生和支持细胞活性的冗余、累加和协同调节发挥作用。此外,支持细胞保留了显著的活性能力,这独立于直接的激素调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b507/2592075/11d3132cc26e/ukmss-2840-f0001.jpg

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