Expression of anti‐Müllerian hormone, CDKN1B, connexin 43, androgen receptor and steroidogenic enzymes in the equine cryptorchid testis

Abstract

Cryptorchidism affects 2-8% of male horses and the affected testis undergoes a disruption of normal spermatogenesis. The underlying molecular changes are poorly understood in the cryptorchid equine testis. Compare the expression of anti-Müllerian hormone (AMH), anti-Müllerian hormone receptor (AMHR2), androgen receptor (AR), cyclin kinase inhibitor (CDKN1B), connexin 43 (Cx43), 3β hydroxysteroid dehydrogenase/Δ(5) -Δ(4) - isomerase (3βHSD), P450c17 hydroxylase/lyase (P450c17) and cytochrome P450 aromatase (P450arom) in the undescended testis of cryptorchid stallions with that of normal stallions. Undescended, abdominal testes from four cryptorchid stallions between 2 and 3 years of age were collected during routine castrations along with normally descended testes from normal stallions between 2 and 3 years of age (n = 7). Samples were analysed by immunohistochemistry and quantitative real-time PCR. Cryptorchid testes had increased AMH and AMHR2 immunolabelling when compared with normal testes, which indicates failure of maturation of Sertoli cells and/or lack of testosterone suppression. Failure of Sertoli cell maturation in the cryptorchid testis may also be attributed to AR abnormalities and/or a consequence of lack of testosterone suppression due to decreased 3βHSD. Cyclin-dependent kinase (CDKN1B) was not expressed in Sertoli cells of cryptorchid testes suggesting that Sertoli cells are still proliferating, which is also a characteristic of the immature testis. In addition, Cx43 expression is decreased in the cryptorchid testis, indicating a disruption in intercellular communication. Undescended testes of cryptorchid horses present characteristics of immaturity suggesting that the failure of Sertoli cell maturation may be a consequence of cryptorchidism. This study provides a better understanding of the effect of cryptorchidism on testicular function in stallions.