The effects of cryptorchidism on the regulation of steroidogenesis and gap junctional communication in equine testes.
Abstract: Evidence collected over the years has demonstrated that cryptorchidism is associated with a defect in spermatogenesis and, as a consequence, with either reduced fertility or infertility. However, the effect of cryptorchidism on Leydig cell function is less clear. The aim of our study therefore was to investigate the regulation of steroid hormone biosynthesis and, additionally, intercellular communication in the cryptorchid equine testes. Methods: Testes of mature bilaterally cryptorchid horse and healthy stallions were used for this study. The expression of luteinising hormone receptor (LHR), 3beta-hydroxysteroid dehydrogenase (3beta-HSD), aromatase and connexin43 (Cx43) was detected by means of immunohistochemistry. Testosterone and oestradiol levels were measured in testicular homogenates using appropriate radioimmunoassays. Results: In the testes of both normal and cryptorchid stallions, immunostaining for LHR, 3beta-HSD and aromatase was confined to the Leydig cells. In the cryptorchid horse, the intensity of the staining for LHR and 3beta-HSD was weaker, whereas the staining for aromatase was clearly stronger than that of the normal stallion. Radioimmunological analysis revealed disturbance of the androgen-oestrogen balance in the cryptorchid testes. Additionally, in both the seminiferous tubules and interstitial tissue of the cryptorchid a clear reduction of the Cx43 signal was observed. Conclusions: Decreased expression of LHR and 3beta-HSD and increased expression of aromatase in the cryptorchid testes suggest that hormonal imbalance was caused both by reduced testosterone synthesis and by increased androgen aromatisation. Impaired expression of Cx43 in the seminiferous tubules as well as in the interstitial tissue of the cryptorchid horse indicates that cryptorchidism affects intercellular communication in the testes.
Publication Date: 2008-05-10 PubMed ID: 18465685
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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The research article investigates the impact of cryptorchidism on hormone regulation and intercellular communication in horse testes, revealing possible hormonal imbalances and communication deficiencies in affected animals.
Objective and Methodology
- The primary aim of the research was to study the changes in steroid hormone biosynthesis and intercellular communication in the cryptorchid equine testes.
- This was carried out by analysing testes of bilaterally cryptorchid horse and healthy stallions (control group).
- The study assessed the expression of luteinising hormone receptor (LHR), 3beta-hydroxysteroid dehydrogenase (3beta-HSD), aromatase and connexin43 (Cx43) using immunohistochemistry.
- The levels of testosterone and oestradiol, two important hormones in the male reproductive system, were measured in testicular homogenates applying radioimmunoassays.
Findings
- In both, normal and cryptorchid testes, LHR, 3beta-HSD, and aromatase were exclusively present in the Leydig cells.
- Compared to healthy stallions, the cryptorchid horses showed weaker staining for LHR and 3beta-HSD, indicating reduced expression of these hormones.
- The staining for aromatase was noticeably stronger in cryptorchid testes, which points to an increased expression of this enzyme responsible for converting androgens into estrogens.
- Radioimmunological analysis highlighted a disruption in the androgen-oestrogen balance in the cryptorchid testes. This indicates a hormonal imbalance.
- There was a significant reduction of the Cx43 signal in both the seminiferous tubules and interstitial tissue of the cryptorchid horse, showing affected intercellular communication within the testes.
Conclusion
- The study’s findings suggest that cryptorchidism causes hormonal imbalance in affected horses due to decreased testosterone synthesis (as evidenced by reduced LHR and 3beta-HSD expressions) and increased androgen aromatisation (indicated by stronger aromatase expressions).
- Also, the paper concludes that cryptorchidism affects the intercellular communication inside the testes, evidenced by the impaired expression of Cx43 in the seminiferous tubules and interstitial tissue of the cryptorchid testes.
Cite This Article
APA
Hejmej A, Bilińska B.
(2008).
The effects of cryptorchidism on the regulation of steroidogenesis and gap junctional communication in equine testes.
Endokrynol Pol, 59(2), 112-118.
Publication
Researcher Affiliations
- Department of Endocrinology and Tissue Culture, Institute of Zoology, Jagiellonian University, Krakow, Poland. a.hejmej@op.pl
MeSH Terms
- 3-Hydroxysteroid Dehydrogenases / biosynthesis
- Animals
- Aromatase / biosynthesis
- Connexin 43 / biosynthesis
- Cryptorchidism / complications
- Estradiol / biosynthesis
- Gap Junctions / metabolism
- Gene Expression
- Horses
- Leydig Cells / metabolism
- Male
- Receptors, LH / biosynthesis
- Spermatogenesis
- Testosterone / biosynthesis
Citations
This article has been cited 13 times.- Khumsap S, Tangtrongsup S, Towiboon P, Somgird C. GnRH Vaccine Could Suppress Serum Testosterone in Stallion Mules. Animals (Basel) 2024 Jun 17;14(12).
- Costagliola A, Montano L, Langella E, Lombardi R, Squillacioti C, Mirabella N, Liguori G. A Comparative Analysis of Orexins in the Physio-Pathological Processes of the Male Genital Tract: New Challenges? A Review. Vet Sci 2024 Mar 15;11(3).
- Liguori G, Tafuri S, Pelagalli A, Ali' S, Russo M, Mirabella N, Squillacioti C. G Protein-Coupled Estrogen Receptor (GPER) and ERs Are Modulated in the Testis-Epididymal Complex in the Normal and Cryptorchid Dog. Vet Sci 2024 Jan 5;11(1).
- Squillacioti C, Pelagalli A, Assisi L, Costagliola A, Van Nassauw L, Mirabella N, Liguori G. Does Orexin B-Binding Receptor 2 for Orexins Regulate Testicular and Epididymal Functions in Normal and Cryptorchid Dogs?. Front Vet Sci 2022;9:880022.
- Lustofin S, Kamińska A, Brzoskwinia M, Cyran J, Kotula-Balak M, Bilińska B, Hejmej A. Nuclear and Membrane Receptors for Sex Steroids Are Involved in the Regulation of Delta/Serrate/LAG-2 Proteins in Rodent Sertoli Cells. Int J Mol Sci 2022 Feb 18;23(4).
- Witkowski M, Pardyak L, Pawlicki P, Galuszka A, Profaska-Szymik M, Plachno BJ, Kantor S, Duliban M, Kotula-Balak M. The G-Protein-Coupled Membrane Estrogen Receptor Is Present in Horse Cryptorchid Testes and Mediates Downstream Pathways. Int J Mol Sci 2021 Jul 1;22(13).
- Assisi L, Pelagalli A, Squillacioti C, Liguori G, Annunziata C, Mirabella N. Orexin A-Mediated Modulation of Reproductive Activities in Testis of Normal and Cryptorchid Dogs: Possible Model for Studying Relationships Between Energy Metabolism and Reproductive Control. Front Endocrinol (Lausanne) 2019;10:816.
- Hollenbach J, Jung K, Noelke J, Gasse H, Pfarrer C, Koy M, Brehm R. Loss of connexin43 in murine Sertoli cells and its effect on blood-testis barrier formation and dynamics. PLoS One 2018;13(6):e0198100.
- Liguori G, Squillacioti C, Assisi L, Pelagalli A, Vittoria A, Costagliola A, Mirabella N. Potential role of orexin A binding the receptor 1 for orexins in normal and cryptorchid dogs. BMC Vet Res 2018 Feb 27;14(1):55.
- Jung HY, Yoo DY, Jo YK, Kim GA, Chung JY, Choi JH, Jang G, Hwang IK. Differential expression of estrogen receptor α and progesterone receptor in the normal and cryptorchid testis of a dog. Lab Anim Res 2016 Jun;32(2):128-32.
- Hermanowicz A, Matuszczak E, Debek W, Dzienis-Koronkiewicz E, Komarowska M, Oksiuta M, Kowalewska J, Milewski R. Expression of estrogen receptors α and β in paratesticular tissues in boys operated on for unilateral cryptorchidism between the 1st and 4th years of life. Med Sci Monit 2012 Oct;18(10):CR630-4.
- Chevallier D, Carette D, Segretain D, Gilleron J, Pointis G. Connexin 43 a check-point component of cell proliferation implicated in a wide range of human testis diseases. Cell Mol Life Sci 2013 Apr;70(7):1207-20.
- Pointis G, Gilleron J, Carette D, Segretain D. Physiological and physiopathological aspects of connexins and communicating gap junctions in spermatogenesis. Philos Trans R Soc Lond B Biol Sci 2010 May 27;365(1546):1607-20.
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