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首页> 外文期刊>Molecular and Cellular Endocrinology >Mouse models of infertility due to swollen spermatozoa.
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Mouse models of infertility due to swollen spermatozoa.

机译:由于精子肿胀而导致的不育小鼠模型。

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摘要

Transgenic mice with male infertility, the c-ros knockout (KO) and GPX5-Tag2 transgenic mouse models, are compared. Both exhibit severely angulated sperm flagella explaining the infertility. As angulated spermatozoa are swollen cells, a failure in volume regulation is indicated. Differences between genotypes were also found: caudal spermatozoa from c-ros KO, but not GPX5-Tag2, could fertilise eggs in vitro; flagellar angulation occurred more within the epididymis of GPX5-Tag2 than c-ros KO mice; the osmotic pressure of cauda epididymidal fluid was lower only in GPX5-Tag2 mice; angulation of caudal sperm from c-ros KO, but not GPX5-Tag2 mice, decreased upon demembranation. These observations indicate that GPX5-Tag2 mice express an earlier, more severe defect. Gene chip analyses of the epididymides revealed decreased expression of the CRES (cystatin-related epididymal-spermatogenic) and MEP17 (murine epididymal protein 17) genes in both genotypes. Further analysis could pinpoint genes essential for epididymal regulation of sperm volume, explain infertility and suggest modes of male contraception.
机译:比较了具有男性不育的转基因小鼠,c-ros基因敲除(KO)和GPX5-Tag2转基因小鼠模型。两者均表现出严重的成角度的精子鞭毛,解释了不育。由于成角的精子是肿胀的细胞,因此指示了体积调节的失败。基因型之间也存在差异:c-ros KO的尾部精子可体外受精,而GPX5-Tag2则不。与c-ros KO小鼠相比,GPX5-Tag2的附睾内鞭毛成角的发生率更高。仅在GPX5-Tag2小鼠中马尾附睾液的渗透压较低。去膜后,来自c-ros KO而非GPX5-Tag2小鼠的尾部精子的成角减小。这些观察结果表明GPX5-Tag2小鼠表达了更早,更严重的缺陷。附睾的基因芯片分析显示两种基因型中CRES(与胱抑素相关的附睾生精)和MEP17(鼠附睾蛋白17)基因的表达均降低。进一步的分析可以查明精子体积附睾调节所必需的基因,解释不育症并建议男性避孕的方式。

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