Testicular Expression of Vitamin-D Receptor and Vitamin-D-Metabolizing Enzymes (CYP2R1, CYP27A1, and CYP27B1) in Normal and Cryptorchid Horses
Vitamin D (VD) is required for testis activity being a key regulator of calcium and testosterone, both essential for spermatogenesis and sperm maturation. VD is activated by a metabolizing machinery of enzymes (CYP2R1, CYP27A1, CYP27B1) and acts throughout its receptor (VDR). Cryptorchidism is a developmental defect caused by the failed scrotal descend of the testicle and can compromise fertility depending on whether one or both testes are retained. Here, we reported the expression and localization of VDR- and VD-activating enzymes in the testis of normal and unilateral cryptorchid equines obtained by Real-Time PCR, Western blotting, and immunohistochemistry. Results demonstrated that cryptorchidism affected gene and protein expression. Leydig cells expressed the highest level of VDR, CYP2R1, CYP27A1, and CYP27B1, whilst CYP27A1 and CYP27B1 were more abundant in spermatids from normal testes compared to scrotal testes of unilateral cryptorchid animals. No different cellular localization of the VD-metabolizing machinery was observed between cryptorchid and scrotal testicles, although some variation in staining intensity was observed. These results provide insights for further studies, required for clarifying VD’s role in equine reproduction.
Authors
- Luca Lacitignola (ORCID: https://orcid.org/0000-0003-4963-8673)
- Antonio Ciro Guaricci (ORCID: https://orcid.org/0009-0008-7985-1743)
- Edmondo Ceci (ORCID: https://orcid.org/0000-0002-5496-4855)
- Maria Albrizio (ORCID: https://orcid.org/0000-0002-8937-3860)
- Mario Cinone (ORCID: https://orcid.org/0000-0002-0495-8975)
- Salvatore Desantis (ORCID: https://orcid.org/0000-0001-8580-7556)
Institutions
- University of Bari Aldo Moro (IT)
Publication Details
- Journal
- Animals
- Published
- 2026-09-28
- DOI
- https://doi.org/10.3390/ani16193046
- Primary Topic
- Vitamin D Research Studies
- Type
- article
- Field-Weighted Citation Impact
- 0.00