Factors involved in the angiogenic process in the testis under chronic inflammation

JACOBO P. V.; SOBARZO C. M.; GUALDONI G.S.; THEAS M. S.; GUAZZONE V. A.; PÉREZ C. V.; LUSTIG L.

CABA

Congreso; Reunión Conjunta de Sociedades de Biociencia; 2017

Experimental autoimmune orchitis (EAO) is an established model of chronic testicular inflammation. The murine model mimics the pathological changes reported in immunological infertility in men. At the end of EAO induction (35 days, d), few signs of inflammation are present in the testis and no damage of seminiferous tubules occurs. At 55d, lymphomononuclear cell infiltrate increases concomitantly with germ cell apoptosis, leading to aspermatogenesis and infertility. Hypoxia and oxidative stress triggers an adaptive response in which hypoxia-inducible factor 1α (HIF1α) and vascular endothelial growth factor (VEGF) are induced. Progression of EAO is associated with an increase of testicular endothelial cells and number of blood vessels. The aim of this study was to explore the role of HIF1α and VEGFA in the angiogenic process that occurs under testicular inflammation. EAO was induced in adult male Wistar rats by active immunization with testis homogenate and adjuvants. Rats were killed on days 35 and 55. Qualitative evaluation of hipoxia showed similar results in EAO vs normal (N) testis (immunohistochemistry, IHQ). HIF1α localized in endothelial and Sertoli cells (IHQ) similarly to VEGFA, as we previously reported. No significant changes in the expression of nuclear HIF1α was observed at 35 and 55d compared to N testis (n= 4-9) (Western blot, Wb). However, VEGFA expression was significantly higher at 35d in testicular fluid vs N rats decreasing at 55d (n= 5-10; p