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Título : | Genetic deletion of Galectin-3 alters the temporal evolution of macrophage infiltration and healing affecting the cardiac remodeling and function after myocardial infarction in mice | Autor : | Cassaglia, Pablo Penas, Federico Betazza, Celeste Fontana Estevez, Florencia Miksztowicz, Verónica Martinez Naya, Nadia Laura Llamosas, María Clara Noli Truant, Sofía Wilensky, Luciana Volberg, Verónica Cevey, Ágata C. Touceda, Vanessa Cicale, Eliana Berg, Gabriela Fernández, Marisa Goren, Nora Morales, Celina González, Germán E. |
Palabras clave : | HERIDAS; GALECTIN 3; MACROFAGOS; INFARTO DEL MIOCARDIO | Fecha de publicación : | 2020 | Editorial : | Elsevier | Cita : | Cassaglia, P., et al. Genetic deletion of Galectin-3 alters the temporal evolution of macrophage infiltration and healing affecting the cardiac remodeling and function after myocardial infarction in mice [en línea]. The American Journal of Pathology. 2020, 190(9) doi:j.ajpath.2020.05.010 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14249 | Resumen : | Abstract: We studied the role of galectin-3 (Gal-3) in the expression of alternative activation markers (M2) on macrophage, cytokines, and fibrosis through the temporal evolution of healing, ventricular remodeling, and function after myocardial infarction (MI). C57BL/6J and Gal-3 knockout mice (Lgals3-/-) were subjected to permanent coronary ligation or sham. We studied i) mortality, ii) macrophage infiltration and expression of markers of alternative activation, iii) cytokine, iv) matrix metalloproteinase-2 activity, v) fibrosis, and vi) cardiac function and remodeling. At 1 week post-MI, lack of Gal-3 markedly attenuated F4/80+ macrophage infiltration and significantly increased the expression of Mrc1 and Chil1, markers of M2 macrophages at the MI zone. Levels of IL-10, IL-6, and matrix metalloproteinase-2 were significantly increased, whereas tumor necrosis factor-α, transforming growth factor-β, and fibrosis were remarkably attenuated at the infarct zone. In Gal-3 knockout mice, scar thinning ratio, expansion, and cardiac remodeling and function were severely affected from the onset of MI. At 4 weeks post-MI, the natural evolution of fibrosis in Gal-3 knockout mice was also affected. Our results suggest that Gal-3 is essential for wound healing because it regulates the dynamics of macrophage infiltration, proinflammatory 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, thus aggravating the evolution of remodeling and function. | URI : | https://repositorio.uca.edu.ar/handle/123456789/14249 | ISSN : | 0002-9440 1525-2191 (online) |
Disciplina: | MEDICINA | DOI: | 10.1016/j.ajpath.2020.05.010 | Derechos: | Acceso abierto |
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