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缺乏ACRBP的小鼠精子在雌性生殖道中的行为。

Behavior of ACRBP-deficient mouse sperm in the female reproductive tract.

作者信息

Nagashima Kiyoshi, Usui Tomoyuki, Baba Tadashi

机构信息

Ph.D. Program in Human Biology, School of Integrative and Global Majors, University of Tsukuba, Ibaraki 305-8577, Japan.

Faculty of Life and Environmental Sciences, University of Tsukuba, Ibaraki 305-8572, Japan.

出版信息

J Reprod Dev. 2019 Apr 12;65(2):97-102. doi: 10.1262/jrd.2018-137. Epub 2018 Dec 29.

Abstract

Gene-knockout mice lacking ACRBP, a proacrosin-binding protein localized in the acrosome of sperm, have been shown to exhibit male subfertility, owing to abnormal formation of the acrosome. In this study, to elucidate the mechanism contributing to the subfertility phenotype, we examined the behavior of ACRBP-deficient mouse sperm in the female reproductive tract. When sperm that had migrated into the uterus and oviduct after mating were counted, the number of ACRBP-deficient sperm was noticeably smaller in the oviduct of mice post mating. However, ACRBP-deficient sperm recovered from the oviduct possessed morphologically normal head shape and retained normal motility. Importantly, ACRBP-deficient sperm displayed a marked reduction in the ability to successfully gain access to unfertilized oocytes. These data suggest that male subfertility of ACRBP-deficient mice may be attributed to incompleteness of the acrosome reaction rather than impairment in sperm migration from the uterus to the oviduct.

摘要

缺乏ACRBP(一种定位于精子顶体的前顶体素结合蛋白)的基因敲除小鼠已被证明由于顶体形成异常而表现出雄性生育力低下。在本研究中,为了阐明导致生育力低下表型的机制,我们检查了ACRBP缺陷型小鼠精子在雌性生殖道中的行为。当对交配后迁移到子宫和输卵管的精子进行计数时,交配后小鼠输卵管中ACRBP缺陷型精子的数量明显较少。然而,从输卵管中回收的ACRBP缺陷型精子头部形态正常,运动能力也正常。重要的是,ACRBP缺陷型精子成功接触未受精卵母细胞的能力显著降低。这些数据表明,ACRBP缺陷型小鼠的雄性生育力低下可能归因于顶体反应不完全,而不是精子从子宫向输卵管迁移的障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ecc/6473115/9a8a36c4cb8f/jrd-65-097-g001.jpg

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