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Serial Enrichment of Spermatogonial Stem and Progenitor Cells SSCs in Culture for Derivation of Long-term Adult Mouse SSC Lines
Published on: February 25, 2013
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FGF9 promotes mouse spermatogonial stem cell proliferation mediated by p38 MAPK signalling
Fan Yang1,2, Eoin C Whelan2, Xuebing Guan1
1State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu, China.
Cell Proliferation
|October 27, 2020
Summary
Fibroblast growth factor 9 (FGF9) promotes spermatogonial stem cell (SSC) proliferation by activating p38 MAPK and increasing Etv5 and Bcl6b expression, crucial for male fertility.
Area of Science:
- Reproductive Biology
- Molecular Endocrinology
- Stem Cell Biology
Background:
- Fibroblast growth factor 9 (FGF9) is produced by testicular somatic cells.
- The precise function of FGF9 in regulating spermatogonial stem cells (SSCs) remains largely uncharacterized.
Purpose of the Study:
- To elucidate the role of FGF9 in the regulation of SSCs.
- To investigate the molecular mechanisms underlying FGF9's effects on SSCs.
Main Methods:
- In vivo Fgf9 overexpression using lentivirus in mouse testes.
- In vitro assessment of FGF9 effects on cultured germ cells and SSCs.
- RNA sequencing (RNA-seq) for gene expression analysis.
- Pharmacological inhibition of p38 MAPK pathway and Etv5 gene knockdown.
Main Results:
- FGF9 overexpression led to spermatogenesis arrest and accumulation of undifferentiated spermatogonia.
- FGF9 treatment significantly increased SSC numbers in vitro.
- FGF9-induced SSC proliferation was dependent on p38 MAPK phosphorylation.
- FGF9 upregulated Etv5 and Bcl6b expression, with Etv5 knockdown abrogating FGF9's growth-promoting effects.
Conclusions:
- FGF9 is a key regulator of SSC proliferation.
- FGF9 exerts its effects via the p38 MAPK pathway.
- FGF9 upregulates Etv5 and Bcl6b, which are critical for SSC expansion.
