Deslorelin influences canine epididymal gene expression of the androgen receptor and prostaglandin metabolism

Deslorelin slow-release implants (DSRI) reversibly suppresses testicular function in dogs, although the effects on the epididymis remain poorly investigated. As prostaglandins E2 and D2 contribute to epididymal function, presumably regulated by androgens, corresponding metabolic enzymes and receptors were examined in an explorative study. Epididymides of three untreated dogs (CG) were compared with five epidymides obtained by unilateral hemicastration after five months of DSRI treatment (TG), and with the recovered epididymis of the other side, collected five months after implant removal (RG). Gene expressions (RT-qPCR) of the androgen receptor (AR), the synthases PTGS2, PTGES, L-PGDS, and H-PGDS, the receptors EP2, EP4, and DP, as well as prostaglandin inactivator HPGD were compared between groups (CG/TG/RG) and epididymal segments (head/body/tail). Protein localization was evaluated immunohistochemically for AR, PTGS2, HPGD, PTGES, EP2, and EP4. Gene expression differed between TG and CG for all genes except for AR (all P < 0.05), with increased expression in the head (PTGS2, HPGD, PTGES, EP4, HPGDS, and DP). Surprisingly, the only significant difference between RG and TG or CG was a higher PTGS2 expression in the tail in CG (P < 0.05). Friedman tests revealed segment-specific gene expressions within TG (DP), RG (AR, HPGD, EP2, EP4, and L-PGDS), and CG (AR, EP2, L-PGDS) (all P < 0.05), indicating segment-specific function, although without significance in post-hoc tests. Specific immunostaining was confirmed in all samples. Unexpectedly, the DSRI did not alter AR expression, but reversibly affected genes expression within the prostaglandin metabolism. Due to the low sample size, this conclusion must be considered preliminary.