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Lcn8 缺乏导致小鼠附睾精子成熟缺陷。

Deficiency for Lcn8 causes epididymal sperm maturation defects in mice.

机构信息

School of Life Science and Key Laboratory of the Ministry of Education for Experimental Teratology, Shandong University, Jinan, 250100, PR China.

Jinan First People's Hospital, Jinan, 250011, PR China.

出版信息

Biochem Biophys Res Commun. 2021 Apr 9;548:7-13. doi: 10.1016/j.bbrc.2021.02.052. Epub 2021 Feb 22.

DOI:10.1016/j.bbrc.2021.02.052
PMID:33631677
Abstract

Lipocalin family members, LCN8 and LCN9, are specifically expressed in the initial segment of mouse caput epididymis. However, the biological functions of the molecules in vivo are yet to be clarified. In this study, CRISPR/Cas9 technology was used to generate Lcn8 and Lcn9 knockout mice, respectively. Lcn8 and Lcn9 male mice showed normal spermatogenesis and fertility. In the cauda epididymis of Lcn8 male mice, morphologically abnormal sperm was increased significantly, the proportion of progressive motility sperm was decreased, the proportion of immobilized sperm was elevated, and the sperm spontaneous acrosome reaction (AR) frequency was increased. Conversely, the knockout of Lcn9 did not have any effect on the ratio of morphologically abnormal sperm, sperm motility, and sperm spontaneous AR frequencies. These results demonstrated the role of LCN8 in maintaining the sperm quality in the epididymis, and suggested that the deficiency of LCN8 leads to epididymal sperm maturation defects.

摘要

脂质运载蛋白家族成员 LCN8 和 LCN9 特异性表达于小鼠附睾头部的初始段。然而,这些分子在体内的生物学功能尚不清楚。在这项研究中,我们分别使用 CRISPR/Cas9 技术生成了 Lcn8 和 Lcn9 敲除小鼠。Lcn8 和 Lcn9 雄性小鼠表现出正常的精子发生和生育能力。在 Lcn8 雄性小鼠的附睾尾部,形态异常的精子显著增加,前向运动精子的比例降低,不动精子的比例升高,精子自发顶体反应(AR)频率增加。相反,Lcn9 的敲除对形态异常精子的比例、精子运动能力和精子自发 AR 频率没有任何影响。这些结果表明 LCN8 在维持附睾精子质量中的作用,并提示 LCN8 的缺乏导致附睾精子成熟缺陷。

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