Animal models of male subfertility targeted on LanCL1-regulated spermatogenic redox homeostasis

Huang, Chao1,2; Yang, Chengcheng1,2; Pang, Dejiang3,4; Li, Chao1,2; Gong, Huan1,2; Cao, Xiyue1,2; He, Xia1,2; Chen, Xueyao1,2; Mu, Bin3,4; Cui, Yiyuan1,2; Liu, Wentao1,2; Luo, Qihui1,2; Cheng, Anchun1,2; Jia, Lanlan1,2; Chen, Mina3,4; Xiao, Bo6; Chen, Zhengli1,2

2022-04-01

10.1038/s41684-022-00961-w

LAB ANIMAL   影响因子和分区

0093-7355

1548-4475

["In this article, the authors identify LanCL1 as a major male germ cell-specific antioxidant gene. Using different mouse models, they show that LanCL1 deficiency results in spermatozoal oxidative damage and impaired male fertility, while LanCL1 transgene expression protects mice against high-fat-diet-induced oxidative damage and subfertility.","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."]

SCI

英语

通讯

National Natural Science Foundation of China[31501200,31871179,32071161] ; Sichuan Provincial Department of Education, China[16ZA0029] ; National Key Technology Support Program of China[2014BAI03B01]

Veterinary Sciences

Veterinary Sciences

WOS:000787163100001

NATURE PORTFOLIO

Web of Science

1.Sichuan Agr Univ, Coll Vet Med, Lab Expt Anim Dis Model, Chengdu, Peoples R China
2.Sichuan Agr Univ, Coll Vet Med, Key Lab Anim Dis & Human Hlth Sichuan Prov, Chengdu, Peoples R China
3.Sichuan Univ, Neurosci & Metab Res State Key Lab Biotherapy, West China Hosp, Chengdu, Peoples R China
4.Collaborat Innovat Ctr, Chengdu, Peoples R China
5.Peoples Hosp Yaan, Clin Lab, Yaan, Peoples R China
6.Southern Univ Sci & Technol, Dept Biol, Shenzhen, Peoples R China

Huang, Chao,Yang, Chengcheng,Pang, Dejiang,et al. Animal models of male subfertility targeted on LanCL1-regulated spermatogenic redox homeostasis[J]. LAB ANIMAL,2022.

Huang, Chao.,Yang, Chengcheng.,Pang, Dejiang.,Li, Chao.,Gong, Huan.,...&Chen, Zhengli.(2022).Animal models of male subfertility targeted on LanCL1-regulated spermatogenic redox homeostasis.LAB ANIMAL.

Huang, Chao,et al."Animal models of male subfertility targeted on LanCL1-regulated spermatogenic redox homeostasis".LAB ANIMAL (2022).