NOVEL INHAT REPRESSOR (NIR) MAY REGULATE VARICOCELE-INDUCED APOPTOSIS THROUGH P53 IN RAT TESTICULAR TISSUE


Akkan S. S., Özbey Ünlü Ö., Bektaş N. İ., Uçak M., Üstünel İ.

15th National and 1st International Congress of Histology and Embryology, Antalya, Türkiye, 26 - 28 Mayıs 2022, ss.80

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: Antalya
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.80
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Introduction: Varicocele is a common cause of male infertility, and lead to oxidative stress. Various studies of

testicular tissues of males with varicocele have shown that apoptosis is increased in developing germ cells. The

P53 plays a role in DNA repair mechanism and induces apoptosis. Nir (novel INHAT repressor) which inhibits

P53-mediated gene transactivation by blocking histon acetylation controls cell proliferation and apoptosis.

Purpose: The apoptotic processes of varicocele still are not known exactly. Currently, there is no evidence of Nir

protein expression in varicocele-induced testicular tissues in any studies. The aim of this study was to investigate

associated of Nir and P53 on testicular damage caused by varicocele.

Material-Method: Thirty male wistar rats were randomly divided into three groups as control, sham and

varicocele (VC). The VC model was established by partial ligation of the left renal vein, and the left testes were

taken from all groups after 13 weeks of varicocele formation. First of all, the obtained sections were stained with

Hematoxylin-Eosin and the degrees of seminiferous tubule degeneration were evaluated under the light

microscope. The TUNEL assay was used to detect apoptotic cells. Nir, p53 and HIF-1α expressions were

determined using Immunohistochemistry and Western blot techniques. One-way ANOVA was used to determine

the statistical significance between the results obtained from the groups.

Results: The expressions of Nir, P53, and HIF-1 were significantly increased (P < 0.05) in the varicocele group

according to the results of Immunohistochemistry and Western blot analysis. In addition, an increase in both

apoptotic germ cell number and seminiferous tubule degeneration was observed in the varicocele group.

Conclusion: In conclusion, increased expression of P53 (as Nir interacting partner) in varicocele group, appears

as a result of varicocele-induced apoptosis. HIF-1α protein which increased with hypoxia in rats with varicocele,

regulates apoptosis-related downstream gene, P53. Increased Nir expression can block P53 activity and therefore

the Nir signaling can play a protective role in this process.