生殖细胞
生物
精子发生
氧化应激
男性不育
转基因
不育
平衡
男科
转基因小鼠
细胞生物学
内分泌学
内科学
遗传学
基因
医学
怀孕
作者
Chao Huang,Chengcheng Yang,Dejiang Pang,Chao Li,Huan Gong,Xiyue Cao,Xia He,Xueyao Chen,Bin Mu,Yiyuan Cui,Wentao Li,Qihui Luo,Anchun Cheng,Lanlan Jia,Mina Chen,Bo Xiao,Zhengli Chen
出处
期刊:Lab Animal
[Springer Nature]
日期:2022-04-25
卷期号:51 (5): 133-145
被引量:2
标识
DOI:10.1038/s41684-022-00961-w
摘要
Oxidative stress in spermatozoa is a major contributor to male subfertility, which makes it an informed choice to generate animal models of male subfertility with targeted modifications of the antioxidant systems. However, the critical male germ cell-specific antioxidant mechanisms have not been well defined yet. Here we identify LanCL1 as a major male germ cell-specific antioxidant gene, reduced expression of which is related to human male infertility. Mice deficient in LanCL1 display spermatozoal oxidative damage and impaired male fertility. Histopathological studies reveal that LanCL1-mediated antioxidant response is required for mouse testicular homeostasis, from the initiation of spermatogenesis to the maintenance of viability and functionality of male germ cells. Conversely, a mouse model expressing LanCL1 transgene is protected against high-fat-diet/obesity-induced oxidative damage and subfertility. We further show that germ cell-expressed LanCL1, in response to spermatogenic reactive oxygen species, is regulated by transcription factor specific protein 1 (SP1) during spermatogenesis. This study demonstrates a critical role for the SP1–LanCL1 axis in regulating testicular homeostasis and male fertility mediated by redox balance, and provides evidence that LanCL1 genetically modified mice have attractive applications as animal models of male subfertility.
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