Role of a PPAR gamma agonist and macrophages in cardiac neovascularization in an experimental model of Chagas? disease

PENAS FEDERICO; CEVEY ÁGATA; GOREN NORA BEATRIZ; MIRKIN GERARDO ADRIAN; SALES MARÍA ELENA; DMYTRENKO GANNA; RADA JIMENA

Mar del Plata

Congreso; LXI REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA (SAIC); 2016

SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA (SAIC)

Chagas disease, caused by Trypanosoma cruzi (Tc), involves a persistent inflammatory response affecting the heart as a main target, where it causes serious alterations. Macrophages (Mp) are involved in the clearance of infection. Upon parasite uptake, Mp increase inflammatory mediators, leading to parasite killing. Yet, inflammatory response exacerbation may lead to tissue damage. PPARg are ligand-dependent nuclear transcription factors that, besides regulating lipid and carbohydrate metabolism, have important anti-inflammatory effects. PPARg has been involved in Mp polarization from M1 to M2 phenotype, yet its role in Tc infection has not been fully elucidated. We evaluated the role of HP24, a synthetic PPARg ligand, in cardiac angiogenesis in an experimental model of Chagas´ disease. HP24 treatment neither changes parasitemia nor survival (P>0.05). Also, body weight remains similar to that of untreated mice. Then, we studied the effect of HP24 in Mp. Treatment increased the expression of VEGFA and Arg I, and decreased the expression of NOS2 as assesed by Western blot (Wb, P