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Busulfan Suppresses Autophagy in Mouse Spermatogonial Progenitor Cells via mTOR of AKT and p53 Signaling Pathways

文献类型： 外文期刊

作者： Wei, Rui 1 ; Zhang, Xiaoyu 1 ; Cai, Yihui 1 ; Liu, Hongyang 1 ; Wang, Bingyuan 2 ; Zhao, Xiaodong 3 ; Zou, Kang 1 ;

作者机构： 1.Nanjing Agr Univ, Coll Anim Sci & Technol, Germline Stem Cells & Microenvironm Lab, Nanjing 210095, Peoples R China

2.Chinese Acad Agr Sci, Inst Anim Sci, Beijing 100193, Peoples R China

3.Shanghai Jiao Tong Univ, Shanghai Ctr Syst Biomed, Key Lab Syst Biomed, Minist Educ, Shanghai 200240, Peoples R China

关键词： Apoptosis; Busulfan; Cell fate; Differential gene expression; Fertility

期刊名称：STEM CELL REVIEWS AND REPORTS （ 影响因子：5.739； 五年影响因子：5.171 ）

ISSN： 2629-3269

年卷期：

页码：

收录情况： SCI

摘要： In testis, a rare undifferentiated germ cell population with the capacity to regenerate robustly and support spermatogenesis, is defined as spermatogonial progenitor cells (SPCs) population. As a widely used drug for tumor therapy or bone marrow transplantation, busulfan has a severe side effect on SPCs population and causes a consequent infertility. Recently, accumulating evidence revealed the protective role of autophagy in stem cell maintenance under exogenous stress. To better understand the role of autophagy in SPCs fates, we investigated the potential function of autophagy in SPCs under busulfan stress, and found that treatment of busulfan induced the formation of autophagic vesicles and autophagosomes in mouse SPCs. Subsequently, a connection of autophagy and SPCs maintenance and survival was demonstrated in a dose-dependent manner. Moreover, mTOR was identified as an essential factor for autophagy in SPCs with a complicated mechanism: (1) mTOR is phosphorylated by AKT to activate its target genes, p70s6 kinase, resulting in the inhibition of autophagy during short-term busulfan treatment. (2) mTOR mediates autophagy with p53 together, to regulate the fate of SPCs. Collectively, observations from this study indicate that moderate autophagy effectively protects SPCs from the stress of chemotherapy, which may provide an important hint for fertility protection in clinic.

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