
Sertoli cell‐derived exosomal MicroRNA‐486‐5p regulates differentiation of spermatogonial stem cell through PTEN in mice
Author(s) -
Li Quan,
Li Hanhao,
Liang Jinlian,
Mei Jiaxin,
Cao Zhen,
Zhang Lei,
Luo Jiao,
Tang Yan,
Huang Rufei,
Xia Huan,
Zhang Qihao,
Xiang Qi,
Yang Yan,
Huang Yadong
Publication year - 2021
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.16347
Subject(s) - microvesicles , sertoli cell , biology , microbiology and biotechnology , cellular differentiation , microrna , pten , exosome , retinoic acid , stem cell , signal transduction , spermatogenesis , cell culture , endocrinology , genetics , gene , pi3k/akt/mtor pathway
Self‐renewal and differentiation of spermatogonial stem cell (SSC) are critical for male fertility and reproduction, both of which are highly regulated by testicular microenvironment. Exosomal miRNAs have emerged as new components in intercellular communication. However, their roles in the differentiation of SSC remain unclear. Here, we observed miR‐486‐5p enriched in Sertoli cell and Sertoli cell‐derived exosomes. The exosomes mediate the transfer of miR‐486‐5p from Sertoli cells to SSCs. Exosomes release miR‐486‐5p, thus up‐regulate expression of Stra8 (stimulated by retinoic acid 8) and promote differentiation of SSC. And PTEN was identified as a target of miR‐486‐5p. Overexpression of miR‐486‐5p in SSCs down‐regulates PTEN expression, which up‐regulates the expression of STRA8 and SYCP3, promotes SSCs differentiation. In addition, blocking the exosome‐mediated transfer of miR‐486‐5p inhibits differentiation of SSC. Our findings demonstrate that miR‐486‐5p acts as a communication molecule between Sertoli cells and SSCs in modulating differentiation of SSCs. This provides a new insight on molecular mechanisms that regulates SSC differentiation and a basis for the diagnosis, treatment, and prevention of male infertility.