新生儿暴露于雌激素改变了成年雄性小鼠生殖道中的蛋白质谱和基因表达

Thierry Normand, Christiane Jean-Faucher, Claude Jean
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引用次数: 9

摘要

在新生儿给予超生理剂量雌二醇后,成年小鼠附睾、输精管和精囊组织蛋白浓度分别显著降低了39%、45%和56%。蛋白质谱显示出持续的改变。在附睾中,4条蛋白带在雌性化雄性中分别增加(14.4、43和67 kDa)或减少(24 kDa)。在输精管中,4种蛋白增加(14.4、49、67和76 kDa), 1种蛋白几乎缺失(34 kDa)。在精囊中,约有20种不同分子量(12-140 kDa)的蛋白质有差异地增加或减少。在成年期,睾酮替代疗法无法逆转这些影响。在成年期用雌二醇治疗会引起3个器官蛋白谱的持续改变,但与新生儿治疗相反,这些改变可以通过雄激素治疗逆转。用从成年精囊中提取的RNA构建cDNA文库,并进行差异杂交筛选。新生雌性激素强烈降低了一些mRNA物种的丰度。共分离出11个含有雌激素敏感序列的重组体。其中2个插入约500个碱基对,用于点印迹杂交。结果表明,这两个克隆含有受雄激素调控的不同序列。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neonatal exposure to oestrogens alters the protein profiles and gene expression in the genital tract of adult male mice

After neonatal administration of supraphysiological doses of oestradiol, the concentration of tissue proteins, in adult mice, was significantly reduced by 39, 45 and 56% in epididymis, vas deferens and seminal vesicle respectively. The protein profiles showed persistent alterations. In epididymis, 4 protein bands were differentially increased (14.4, 43 and 67 kDa) or reduced (24 kDa) in oestrogenized males. In vas deferens, 4 proteins were increased (14.4, 49,67 and 76 kDa) and one (34 kDa) virtually absent. In seminal vesicle, about 20 proteins of varying molecular weights (12–140 kDa) were differentially increased or decreased. Testosterone substitution, at adulthood, was unable to reverse these effects. Treatments with oestradiol during adult life induced persistent alterations in the protein profiles of the 3 organs but, in contrast to neonatal treatment, these alterations could be reversed by androgen therapy. A cDNA library has been constructed with RNA prepared from adult seminal vesicle and screened by differential hybridization. Neonatal oestrogenization strongly reduced the abundance of some mRNA species. Eleven recombinants containing putative oestrogen-sensitive sequences were isolated. Two of them, having an insert of about 500 base pairs, were used for dot-blot hybridization. Results showed that the two clones contained sequences which were differently regulated by androgens.

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