MALCHIODI Emilio Luis
Galectin 3 is essential for the early wound healing and ventricular remodelin after myocardial infartion in mice.
GONZÁLEZ GE; CASSAGLIA P; NOLI TRUANT S; FERNÁNDEZ MM; WILENSKY L; VOLBERG V; MALCHIODI EL; MORALES C; GELPI RJ
INTERNATIONAL JOURNAL OF CARDIOLOGY
ELSEVIER IRELAND LTD
Lugar: Amsterdam; Año: 2014 vol. 176 p. 1423 - 1425
Healing after myocardial infarction (MI) is a well-orchestrated time-dependent process that involves inflammation, tissue repair with progressive extracellular collagen matrix (ECM) deposition and scar formation. This scar should provide an adequate tensile strength to prevent the expansion, subsequent ventricular dilation , adverse ventricular remodeling (VR) and dysfunction . Conversely, a defect in the healing process or an increase in the infarct size and parietal stress are major determinants to enhance the expansion and risk of adverse clinical outcomes, failure and death. Therefore, the idea to modify such an inflammatory process in order to revert the unfavorable course of VR post MI is still under debate [3,4] . Galectin-3 (Gal-3) is a b-galactoside-binding lectin widely expressed in the immune system. Classically, macrophages have been considered as the main source of Gal-3 . Previous studies asserted that this lectin is up-regulated under different pathological conditions and stimulates inflammation and fibrosis[5,6]. Studies in-vivo showed that the infusion of Ang II increases the cardiac expression of Gal-3, suggesting that the pro-inflammatory effect of Ang II may be partially mediated by Gal-3. It has also been demonstrated that Gal-3 stimulate myocardial infiltration and phagocytic activity of macrophages, causing (or cause) myocarditis, fibrosis and ventricular dysfunction [5,6]. During the last few years, plasma levels of Gal-3 were proposed as a strong prognostic marker of cardiac failure  and Mayr et al. recently showed that those levels correlated to the size of the MI in patients . In rats with MI, Gal-3 reached its highest level of expression in the MI area after 7 days of evolution  suggesting that it could stimulate the post MI repair process. However, whether Gal-3 contributes or affects the well-orchestrated healing process after MI is not known. We hypothesize that the lack of Gal-3 prevents macrophage infiltration at the onset of the healing process, decreases the collagen deposition, and contributes to the adverse remodeling development after MI in mice. Accordingly, the aim was to study whether the lack of Gal-3 reduces the macrophage infiltration and fibrosis, therefore modifying the remodeling, the ventricular function, and the infarct size in Gal-3 KO mice.