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miR‐100 promotes the proliferation of spermatogonial stem cells via regulating Stat3
Author(s) -
Huang YongLi,
Huang GuanYou,
Lv Jing,
Pan LiNa,
Luo Xi,
Shen Jie
Publication year - 2017
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.22843
Subject(s) - biology , gene silencing , microrna , microbiology and biotechnology , stat3 , downregulation and upregulation , cell growth , spermatogenesis , stem cell , signal transduction , gene , genetics , endocrinology
Micro RNAs play important roles during mammalian spermatogenesis, but the function(s) of specific miRNAs remain largely unknown. Here, we report that miR‐100 is predominantly expressed in undifferentiated murine spermatogonia, including spermatogonial stem cells (SSCs). We utilized a miRNA mimic and inhibitor to knock down and overexpress miR‐100 in cultured SSCs, respectively, finding that the miR‐100 promotes the proliferation of SSCs in vitro. Furthermore, signals promoting SSC maintenance induced, whereas retinoic acid repressed, expression of miR‐100. Stat3 expression was modulated by miR‐100, with increased transcript and protein abundance in the presence of the miR‐100 inhibitor versus reduced protein levels following miR‐100 overexpression. Stat3 silencing also mimicked the reduced SSC proliferation phenotype associated with elevated miR‐100 levels. Importantly, Stat3 silencing rescued the anti‐proliferation capacity of miR‐100 inhibitor on cultured SSCs. Given that the Stat3 3′ untranslated region was not repressed by pre‐miR‐100 in a standard luciferase reporter assay, we suggest that miR‐100 promotes SSC proliferation by indirect regulation of Stat3 .