PRSS50-mediated inhibition of MKP3/ERK signaling is crucial for meiotic progression and sperm quality

作者：Chunxue Niu, 东北师范大学药物基因与蛋白筛选国家工程实验室, 吉林 长春 130117, 中国, Jiawei Li, Xiaoli Li, Linlin Zhang, Lang Yan, Zhenbo Song, Chunlei Yu, Xiaoguang Yang, Haifeng Zhao, Jialing Sun, Lihua Zheng, Xue Wang, Ying Sun, Xiaohong Han, Guannan Wang, Yongli Bao, 东北师范大学国际人类干细胞库联合研究中心, 吉林 长春 130117, 中国, 吉林省药品检验所, 吉林 长春 130022, 中国 · 发表于：动物学研究 · 年份：2024 · DOI：10.24272/j.issn.2095-8137.2023.388 · 被引用次数：5 · 研究领域：Sperm and Testicular Function、Reproductive Biology and Fertility、Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities

Previous study has found that PRSS50 (TSP50) is highly expressed in spermatocytes, and our study aims to investigate its role in testicular development and spermatogenesis. We first found that PRSS50 knockdown hindered DNA synthesis of spermatocytes. Then we generated Prss50-/- (PRSS50 knockout) mice and found that it exhibited abnormal compression of spermatid nucleus and reduced male fertility. Furthermore, dysplasia of seminiferous tubules along with lower levels of sex hormones were observed in 4-week-old Prss50-/- mice accompanied by defects in meiotic progression and excessive apoptosis of spermatogenic cells. Mechanistic analysis suggested that PRSS50 deletion increased phosphorylation of ERK1/2 and the level of MKP3, a specific antagonist of ERK, which may account for testicular dysplasia in adolescent Prss50-/- mice. Taken together, our results indicate that PRSS50 plays an important role in testicular development and spermatogenesis, and MKP3/ERK signal is involved in this process.