Deficiency of fibroblast growth factor (FGF-2) leads to abnormal spermatogenesis and altered sperm physiology

SAUCEDO L; RUMPEL L; SOBARZO C; SCHREINER D; BRANDES G; LUSTIG L; VAZQUEZ-LEVIN M; GROTHE C; MARÍN-BRIGGILER C

JOURNAL OF CELLULAR PHYSIOLOGY

WILEY-LISS, DIV JOHN WILEY & SONS INC

Lugar: New York; Año: 2018

0021-9541

Fibroblast Growth Factor 2 (FGF2) and its receptors (FGFRs) have been described inseveral tissues, where they regulate cellular proliferation, differentiation, motility and apoptosis. However, there is scarce evidence on their expression in the reproductive tract and gametes, and their involvement in the maintenance of sperm function. The objectives of the present study were to determine the presence of FGF2 in the female reproductive tract and to assess the role of the FGF2/FGFRs system in the regulation of sperm physiology using the murine model. FGF2 was detected in uterus and oviduct protein extracts, and it was localized in epithelial cells of the uterus, isthmus and ampulla, as well as in the cumulus oophorus‐oocyte complex. The receptors FGFR1, FGFR2, FGFR3 and FGFR4 were found to be expressed in cauda epididymal sperm, and were immunodetected in the flagellum and acrosomal region. Analysis of testis sections showed the expression of FGFRs in germ cells atdifferent stages of the spermatogenesis, suggesting the testicular origin of the sperm receptors. Incubation with recombinant FGF2 (rFGF2) led to an enhancement in sperm motility and to an increase in sperm intracellular Ca2+ levels and acrosomal loss compared to the control. In conclusion, this study shows that FGF2 is expressed in tissues of the female reproductive tract, that functional FGFRs are present in mouse sperm, and that rFGF2 affects sperm motility and acrosomal exocytosis, suggesting that this system is involved in the in in the in vivo maintenance of sperm function.