1. Involvement of c-Src/STAT3 signal in EGF-induced proliferation of rat spermatogonial stem cells
- Author
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Jia-Xiang Chen, Jinglei Wang, Xin-Chang Wang, Lin-Lin Xu, and Hai-yan Qin
- Subjects
Male ,STAT3 Transcription Factor ,Cell Survival ,Clinical Biochemistry ,Biology ,CSK Tyrosine-Protein Kinase ,Epidermal growth factor ,medicine ,Animals ,Humans ,Viability assay ,Phosphorylation ,STAT3 ,Molecular Biology ,Cell Proliferation ,Gene knockdown ,Epidermal Growth Factor ,Stem Cells ,Cell Biology ,General Medicine ,Protein-Tyrosine Kinases ,Molecular biology ,Spermatogonia ,Cell biology ,Rats ,medicine.anatomical_structure ,src-Family Kinases ,STAT protein ,biology.protein ,Stem cell ,Germ cell ,Proto-oncogene tyrosine-protein kinase Src ,Signal Transduction - Abstract
Epidermal growth factor (EGF) plays a role in male germ cell development, but the precise function is yet to be defined. This study shows that EGF stimulates rat spermatogonial proliferation in a dose-dependent manner and significantly increased the protein levels of phosphated c-Src (p-c-Src) and phosphated signal transducer and activator of transcription 3 (p-STAT3). Moreover, overexpression of c-Src tagged with enhanced green fluorescence protein (EGFP) in rat spermatogonial stem cells enhances the cell viability. In contrast, knockdown or inhibition of c-Src inhibits rat spermatogonial stem cell proliferation; EGF could not abrogate the inhibitory effect. Evidently, the content of p-STAT3 protein was increased in c-Src-expressing cells and decreased in c-Src-suppressing cells. Furthermore, knockdown or inhibition of STAT3 also suppressed cell viability; neither EGF nor increased c-Src could reverse the inhibitory effect. These results are the first evidence that EGF induces proliferation of rat spermatogonial stem cells through c-Src/STAT3 signal.
- Published
- 2011