Deficiency of Fibroblast Growth Factor 2 (FGF-2) leads to abnormal spermatogenesis and altered sperm physiology

SAUCEDO L; RUMPEL, R; SOBARZO, C; SCHREINER, D; BRANDES, G; LUSTIG, L.; VAZQUEZ LEVIN MH,; GROTHE, C; MARIN BRIGGILER, CI

JOURNAL OF CELLULAR PHYSIOLOGY

WILEY-LISS, DIV JOHN WILEY & SONS INC

Lugar: New York; Año: 2018

0021-9541

Previous studies from our laboratory have shown the presence of Fibroblast Growth Factor 2 (FGF-2) and its receptors (FGFRs) in human testis and sperm, and the results suggest that this system is involved in the regulation of human spermatogenesis and sperm motility. The aim of the present study was to analyze the role of FGF-2 in the maintenance of sperm physiology using FGF-2 knockout (KO) mice. Our results have shown that in wild type (WT) animals, FGF-2 is expressed in germ cells of the seminiferous epithelium (with higher expression in elongating/elongated spermatids) and in epithelial cells of the epididymis. The protein was also immunolocalized in the flagellum and acrosomal region of epididymal sperm. In the FGF-2 KO mice, the analysis of the seminiferous tubules revealed alterations in spermatogenesis kinetics. Additionally, these animals presented higher numbers of spermatids per testis and enhanced daily sperm production compared to the WT males. No difference in the percentage of sperm motility was detected between WT and KO mice, but a significant increase in sperm concentration and in sperm head abnormalities was observed in FGF-2 KO animals. Sperm from KO mice depicted reduced phosphorylation on tyrosine residues (a phenomenon that was associated with sperm capacitation) and increased acrosomal loss after incubation under capacitating conditions. In FGF-2 KO sperm, acrosomal instability was also evidenced by electron microscopy studies. However, the FGF-2 KO males displayed no apparent fertility defects, since their mating with WT females showed no differences in the time to delivery, litter size and pup weight in comparison to WT males. Overall, our findings indicate that FGF-2 exerts a role in mammalian spermatogenesis, and that the lack of this factor leads to dysregulated sperm production and altered sperm physiology. FGF-2-deficient mice constitute a model for the study of the complex mechanisms underlying mammalian spermatogenesis.