Genetic mutation of Galectin-3 altered the temporal evolution of macrophages polarization and healing affecting the post myocardial infarct remodeling in mice.

FEDERICO PENAS; WILENSKY L; MIKSZTOWICZ V; BERG G; CELINA MORALES C; PABLO CASSAGLIA; BETTAZZA C; NOLI TRUANT, SOFIA; CICALE E; GOREN N; GERMÁN E. GONZALEZ; MARTÍNEZ NAYA N; FONTANA ESTEVEZ F; CEVEY A; FERNÁNDEZ MARISA MARIEL

París

Congreso; 2019 European Society of Cardiology Congress.; 2019

European Society of Cardiology

Background: Myocardial infarction (MI) is a dynamic process that leads to ventricularremodeling (VR) and heart failure (HF). Previous studies established that Galectin-3 (Gal-3), is increased during infarction and it is a prognostic marker of HF.Purpose: we aimed tostudy the effects of genetic mutation of Gal-3 on macrophages (MΦ) infiltration, cytokinesexpression, fibrosis and MMP-2 activity as well as, VR and function after MI in mice.Methods: male C57BL/6J and Gal-3 knockout (KO) mice were subjected to permanentcoronary ligature or sham. At 1 week post-MI we studied in the infarct zone: 1) F4/80+ MΦinfiltration by flow cytometry; 2) M1/M2 macrophage polarization by detection of mannosereceptor (MR) and chitinase-3-like protein-3 (YM1) phenotype markers by rt-qPCR; 3)mRNA expression of TNF-, IL-6, IL-10 and TGF-; 4) MMP-2 activity by zymography; 5)fibrosis at the infarct zone by histology. LV function and remodeling were studied byechocardiography. Results: are expressed as X±SEM; * p