Fibroblast Growth Factor 9 Promotes Rat Leydig Cell Development via H3K4me3 Histone Modifications.

Authors

Hehua Quan, Jiayi He, Feilu Wang, Yubin Xu, Huiqian Zhang, Qingyuan Wang, Ren-Shan Ge, Xiaoheng Li

Published in

Reproduction (Cambridge, England). Jun 19, 2026. Epub Jun 19, 2026.

Abstract

Fibroblast Growth Factor 9 (FGF9), as one of the fibroblast growth factor family, is vital for testis formation. Additionally, histone modifications, especially H3K4me3, have been reported to be important in steroidogenesis. However, the regulation of SLC differentiation by FGF9 and the role of histone modifications in this process remain unclear. Adult male Sprague-Dawley rats were treated with ethane dimethane sulfonate to deplete LCs, followed by intratesticular injection of FGF9 from post EDS day 14 to 28 at 0, 10, and 100 ng/testis. qPCR and Western blot analyses were used to detect the gene expression and protein levels of testosterone(T) synthesis. ChIP-seq was employed to identify the H3K4me3-binding regions and binding levels. The results showed that FGF9 treatment led to an increase in serum T levels, LC number and the expression of LC-specific genes (Lhr, Scarb1, Stard1, Cyp11a1, Cyp17a1, Hsd17b3, and Hsd11b1). FGF9 markedly increased H3K4me3 protein levels and decreased H3K9me3 protein level. FGF9 promoted H3K4me3 on the promoter regions of Scarb1, Stard1 and Srd5a1 in vivo. In vitro studies demonstrated that FGF9 increased medium T levels and stimulated the incorporation of EdU, a marker of cell proliferation, into stem LCs after tubule culture. Moreover, Fgfr1 siRNA and WDR5-0103, the histone methyltransferases, could reverse the effect of FGF9 on promoting T production. This study supports previous ones demonstrating that FGF9 stimulates the proliferation and differentiation of stem LCs in an EDS-treated model and in vitro tubule culture model through H3K4me3 histone modifications.

PMID:
42320039
Bibliographic data and abstract were imported from PubMed on 20 Jun 2026.

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