Background: Undescended testis (UDT) causes an increased risk of infertility and malignancy resulting from aberrant germ cell (GC) development. Androgens are proposed to control early GC development.
Objective: To assess the effect of androgen on perinatal GC development in mice.
Material and Methods: Testes from androgen receptor knockout (ARKO) mice and wildtype (WT) littermates (n=3/group) were collected at embryonic (E) day 17 (day of virginal plug = E0), postnatal (P) days P0 (birth), P2, P4, P6, P8 and P10 for immunohistochemistry. Antibodies against mouse VASA homologue (MVH, GC marker), anti-Műllerian hormone (AMH, Sertoli cell marker), Ki-67 (proliferating cell marker), and DAPI (cell nuclei) were used and visualised by confocal microscopy. The numbers of GC/tubule, GC on the tubular basement membrane (GC/BM), Sertoli cells/tubule and the percentage of proliferating GC (Ki67+)/tubule and GC (Ki67+)/BM were counted. Data were analysed using t-test with software GraphPad Prism 5.02.
Results: In WT testes, GC/tubule decreased from E17 to P2, and then increased normally up to P10. Number of MVH + GC/tubule and GC on the BM were similar in ARKO and WT testes (p>0.05) at all time points. In addition, the percentages of proliferating GC (Ki-67+)/tubule and proliferating GC (Ki67+)/BM were similar at all time points (p>0.05) between ARKO and WT testes.
Conclusion: These results show that androgen does not control normal proliferation and migration of gonocytes from the centre of testicular tubules to BM, and putative transformation into type A spermatogonia, between birth and day 10 in mice. As this time interval spans normal ‘minipuberty’, which occurs between day 2 and day 6 in mice, it suggests that during murine minipuberty a novel, non-androgenic factor may stimulate early GC development. Identifying such a non-androgenic factor might be important for future medical therapy to improve fertility potential of boys with UDT and undergoing orchidopexy.