Genetic Deletion of Galectin-3 Altered the Temporal Evolution of Macrophage Infiltration and Healing Affecting the Cardiac Remodeling and Function After Myocardial Infarction in Mice

CASSAGLIA, PABLO; ESTEVEZ, FLORENCIA FONTANA; LLAMOSAS, MARÍA CLARA; VOLBERG, VERÓNICA; CICALE, ELIANA; GOREN, NORA; CASSAGLIA, PABLO; ESTEVEZ, FLORENCIA FONTANA; LLAMOSAS, MARÍA CLARA; VOLBERG, VERÓNICA; CICALE, ELIANA; GOREN, NORA; PENAS, FEDERICO; MIKSZTOWICZ, VERÓNICA; TRUANT, SOFÍA NOLI; CEVEY, ÁGATA C.; BERG, GABRIELA; MORALES, CELINA; PENAS, FEDERICO; MIKSZTOWICZ, VERÓNICA; TRUANT, SOFÍA NOLI; CEVEY, ÁGATA C.; BERG, GABRIELA; MORALES, CELINA; BETTAZZA, CELESTE; NAYA, NADIA MARTÍNEZ; WILENSKY, LUCIANA; TOUCEDA, VANESSA; FERNÁNDEZ, MARISA; GONZÁLEZ, GERMÁN E.; BETTAZZA, CELESTE; NAYA, NADIA MARTÍNEZ; WILENSKY, LUCIANA; TOUCEDA, VANESSA; FERNÁNDEZ, MARISA; GONZÁLEZ, GERMÁN E.

AMERICAN JOURNAL OF PATHOLOGY

AMER SOC INVESTIGATIVE PATHOLOGY, INC

Lugar: Bethesda ; Año: 2020 p. 1789 - 1800

0002-9440

We studied the role of Gal-3 in the expression of alternative activation markers (M2) on macrophage, cytokine expression and fibrosis through the temporal evolution of healing, ventricular remodeling and function after myocardial infarction (MI) in mice. Male C57BL/6J and Gal-3KO mice were subjected to permanent coronary artery ligation or sham for 1 and 4 weeks. We studied: 1) mortality; 2) macrophage infiltration and expression of markers of alternative activation at the infarct zone; 3) cytokine expression; 4) MMP-2 activity; 5) fibrosis; 6) cardiac function and remodeling. At 1 week post-MI, lack of Gal-3 markedly attenuated F4/80+ macrophages infiltration at the infarct zone with increased expression of mannose receptor and YM1, markers of M2 macrophages. Levels of IL-10 and IL-6 and MMP-2 activity were significantly increased whereas TNF-α, TGF-β and fibrosis were remarkably attenuated at the infarct zone. In Gal-3KO mice, scar thinning ratio and expansion, cardiac remodeling and function, were severely affected from the onset of MI. At 4 weeks post-MI, the natural evolution of fibrosis in Gal-3KO mice was also affected. Our results suggest that Gal-3 is essential for wound healing since it regulates the dynamics of macrophage infiltration, pro- and anti-inflammatory cytokine expression and fibrosis along the temporal evolution of MI in mice. The deficit of Gal-3 affected the dynamics of wound healing aggravating thus the evolution of remodeling and function.