Deficiency of NR2C2 accelerates senescence of testicular Leydig cells and infertility in male mice.

Dalian Gong, Zhihui Liu, Rongda Kang, Xiaowen Liu, Ziqian Min, Huan Xin, Yanan Liu, Yuanyuan Chen, Min Liu, Ying Liang, Anji Chen, Lifang Yang, Zenghui Mao, Dan Li

Hunan Research Center of the Basic Discipline for Cell Signaling, College of Biology, Hunan University, Changsha 410082, China.Hunan Research Center of the Basic Discipline for Cell Signaling, College of Biology, Hunan University, Changsha 410082, China. · pubmed

Paper

Abstract

The Leydig cell is one of the components that make up the testicular microenvironment, playing a crucial role in male reproductive function by secreting androgens and cytokines. The present study found that knocking down NR2C2, a member of the 2C group of the nuclear receptor family, can lead to senescent phenotype in mouse primary Leydig cells, with increased cell apoptosis and DNA damage, enhanced SA-β-Gal activity, and decreased glutathione levels. The fertility of Nr2c2 heterozygous knockout mice (Nr2c2

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Research summary

Knocking down NR2C2 leads to senescence in Leydig cells, contributing to infertility in male mice. The study addresses the cellular mechanisms of aging in a specific cell type, which is relevant to understanding the aging process and its impact on reproductive health.

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