HP24 regulates pro-inflammatory and pro-angiogenic mediators by PPARγ -dependent and -independent mechanisms in T. cruzi infected macrophages

FEDERICO PENAS; GERARDO ARIEL MIRKIN,; GOREN, NORA; DAVIDE CARTA; MARÍA ELENA SALES,; CEVEY AGATA; MARIA GRAZIA FERLIN

Mar del Plata

Congreso; LXIII Reunión Anual de la Sociedad Argentina de Investigación Clínica-LXVI Reunión Anual de la Sociedad Argentina de Inmunología-Reunión Anual de la Sociedad Argentina de Fisiología.; 2018

SAIC SAI SAFIS

Chagas disease is caused by T. cruzi infection and represents amajor public health problem in Latin America. Macrophages (MΦ)are one of the main infiltrating leukocytes arriving early to the myocardiumin response to the infection. They persist as an importantimmune cell population in the heart of patients with chronic Chagasdisease. HP24, a 3-hydroxy-4-piridinecarboxylic acid derivative,is a new PPARγ ligand. It exerts significant anti-inflammatory andpro-angiogenic effects. In this work, we analyzed whether HP24 exertsits effects through PPARγ-dependent or -independent mechanismsin T. cruzi infected macrophages. For this purpose, we usedspecific knock-down of this nuclear receptor, by small interferingRNA (PPARγ siRNA). In the absence of PPARγ, HP24 was unableto exert its anti-inflammatory effects on NOS2 expression (Wb andICQ) and NO release (Griess method) (P