Hui Zhou1, Cong Shen2, Yueshuai Guo3, Xiaoyan Huang3, Bo Zheng4, Yibo Wu5. 1. Human Reproductive and Genetic Center, Affiliated Hospital of Jiangnan University, Wuxi, 214122, China. 2. State Key Laboratory of Reproductive Medicine, Center for Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou, 215002, China. 3. State Key Laboratory of Reproductive Medicine, Department of Histology and Embryology, Nanjing Medical University, Nanjing, 211166, China. 4. State Key Laboratory of Reproductive Medicine, Center for Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou, 215002, China. bozheng@njmu.edu.cn. 5. Human Reproductive and Genetic Center, Affiliated Hospital of Jiangnan University, Wuxi, 214122, China. moliaty@aliyun.com.
Abstract
BACKGROUND: Spermatogonial stem cells (SSCs) are unique stem cells that account for the whole reproductive life of males and transmit genetic information to offspring. SSC maintenance is intricate and the underlying mechanisms are largely unclear. Here, we report that SSC maintenance is driven by the plasminogen receptor (PLGRKT). METHODS AND RESULTS: PLGRKT was located in SSCs, and knockdown of PLGRKT expression in cultured neonatal testis and SSCs impaired the proliferation and promoted the apoptosis of cells. PLGRKT interacted with B lymphoma Mo-MLV insertion region 1 (BMI1), and modulated oxidative stress and p16/p19 signaling in SSCs. CONCLUSIONS: We demonstrated that reactive oxygen species (ROS) and p16/p19 signaling are involved in "PLGRKT-BMI1" co-regulation of SSC maintenance in mice.
BACKGROUND: Spermatogonial stem cells (SSCs) are unique stem cells that account for the whole reproductive life of males and transmit genetic information to offspring. SSC maintenance is intricate and the underlying mechanisms are largely unclear. Here, we report that SSC maintenance is driven by the plasminogen receptor (PLGRKT). METHODS AND RESULTS: PLGRKT was located in SSCs, and knockdown of PLGRKT expression in cultured neonatal testis and SSCs impaired the proliferation and promoted the apoptosis of cells. PLGRKT interacted with B lymphoma Mo-MLV insertion region 1 (BMI1), and modulated oxidative stress and p16/p19 signaling in SSCs. CONCLUSIONS: We demonstrated that reactive oxygen species (ROS) and p16/p19 signaling are involved in "PLGRKT-BMI1" co-regulation of SSC maintenance in mice.
Authors: Saher Sue Hammoud; Diana H P Low; Chongil Yi; Douglas T Carrell; Ernesto Guccione; Bradley R Cairns Journal: Cell Stem Cell Date: 2014-05-15 Impact factor: 24.633