BMPR-IB Modulates Steroidogenic Enzyme Genes Differentially in Pubertal and Adult Male Mice — ASN Events

BMPR-IB Modulates Steroidogenic Enzyme Genes Differentially in Pubertal and Adult Male Mice (#161)

Ilona M. Ciller 1 , Ursula A. Ciller 1 , Suresh K. A. Palanisamy 1 , Ibtisam A. N. Al-Ali 1 , Jim R. McFarlane 1
  1. Centre for Bioactive Discovery in Health and Ageing, University of New England, Armidale, NSW, Australia

In males pituitary gonadotrophin signaling up-regulates testicular steroid production and male germ cell development. Transforming growth factor-β (TGF-β) superfamily members such as bone morphogenetic proteins (BMPs) and their receptors have been shown to modulate this process. We have previously reported that BMPR-IB immunization increased basal testosterone in mature males but not pubertal testosterone while eCG stimulated testosterone was not significantly different in either groups. Therefore, in this study we investigated the role of BMPR‑IB on testicular expression of key steroidogenic enzymes in pubertal and mature mice vaccinated against BMPR-IB.

Male mice aged 21 and 56 days were passively immunized with anti-BMPR‑IB in 100ul of PBS by subcutaneous injections with and without equine chorionic gonadotrophin (eCG) to override endogenous gonadotrophins. The preparations were administered daily for six days. On the seventh day mice were sacrificed by asphyxiation with CO2 and the testes removed and prepared for ribonucleic acid (RNA) extraction. To determine the relative expression patterns of Cyp19, Hsd3b1, Hsd3b6 and Hsd17b3, we performed total RNA extractions and quantification followed by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Real time gene amplification results were analysed using beta-actin as the control.

In adult mouse testis BMPR-IB immunization decreased Cyp19 and Hsd3b6, and increased Hsd3b1 while having no affect in pubertal testis. In pubertal testis eCG increased the expression of Hsd3b1 and decreased Hsd3b6 while having the opposite effect in adults. We conclude that BMPR-IB modulates testosterone using a cellular pathway distinctly different from the gonadotrophins. We also conclude that BMPR-IB enhances aromatase production in males which is very similar to the role of BMPR-IB reported in the female ovary.