FACTORS INVOLVED IN THE ANGIOGENIC PROCESS IN THE TESTIS UNDER CHRONIC INFLAMMATION

JACOBO PV; PÉREZ CV; GUALDONI GS; SOBARZO CM; LUSTIG L; GUAZZONE VA; THEAS MS

CABA

Congreso; I Reunión Conjunta de Sociedades Biomédicas; 2017

Experimental autoimmune orchitis (EAO) is an established modelof chronic testicular inflammation. The murine model mimics thepathological changes reported in immunological infertility in men. Atthe end of EAO induction (35 days, d), few signs of inflammation arepresent in the testis and no damage of seminiferous tubules occurs.At 55d, lymphomononuclear cell infiltrate increases concomitantlywith germ cell apoptosis, leading to aspermatogenesis and infertility.Hypoxia and oxidative stress triggers an adaptive response inwhich hypoxia-inducible factor 1α (HIF1α) and vascular endothelialgrowth factor (VEGF) are induced. Progression of EAO is associatedwith an increase of testicular endothelial cells and number ofblood vessels. The aim of this study was to explore the role of HIF1αand VEGFA in the angiogenic process that occurs under testicularinflammation. EAO was induced in adult male Wistar rats by activeimmunization with testis homogenate and adjuvants. Rats werekilled on days 35 and 55. Qualitative evaluation of hipoxia showedsimilar results in EAO vs normal (N) testis (immunohistochemistry,IHQ). HIF1α localized in endothelial and Sertoli cells (IHQ) similarlyto VEGFA, as we previously reported. No significant changes in theexpression of nuclear HIF1α was observed at 35 and 55d comparedto N testis (n= 4-9) (Western blot, Wb). However, VEGFA expressionwas significantly higher at 35d in testicular fluid vs N rats decreasingat 55d (n= 5-10; p