4.6 Article

Transcriptomic Analysis of Testicular Gene Expression in a Dog Model of Experimentally Induced Cryptorchidism

Journal

CELLS
Volume 11, Issue 16, Pages -

Publisher

MDPI
DOI: 10.3390/cells11162476

Keywords

cryptorchidism; tight junction; claudin; sertoli cell; dog

Categories

Funding

  1. National Research Foundation of Korea (NRF), Korean government (MIST) [2021R1G1A1091690]
  2. National Research Foundation of Korea [2021R1G1A1091690] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Cryptorchidism may affect Claudin expression, which in turn impacts the proliferation of Sertoli cells and spermatogenesis.
Cryptorchidism, a condition in which testes fail to descend from the abdomen into the scrotum, is a risk factor for infertility and germ cell cancer. Normally, tight junctions between adjacent Sertoli cells in the testes form a blood-testes barrier that regulates spermatogenesis; however, the effect of cryptorchidism on tight junctions is not well-understood. We established a model of heat-induced testicular damage in dogs using surgical cryptorchidism. We sequenced RNA to investigate whether certain transcripts are expressed at higher rates in heat-damaged versus normally descended testes. Claudins, cell adhesion molecules, were relatively highly expressed in cryptorchid testes: claudins 2, 3, 5, 11, and 18 were significantly increased in cryptorchid testes and reduced by orchiopexy. SOX9-positive Sertoli cells were present in the seminiferous tubules in both cryptorchid and control testes. Using real-time PCR and Western blot analysis to compare Sertoli cells cultured at 34 degrees C and 37 degrees C, we found that Sertoli cell claudins 2, 3, 5, 11, and 18 were significantly increased at 37 degrees C; however, accumulation was higher in the G0/G1 phase in Sertoli cells cultured at 34 degrees C. These results indicate that testicular hyperthermia caused by cryptorchidism affects claudin expression, regulated germ cell death, and the proliferation of Sertoli cells.

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