Genetic deletion of Galectin-3 reduced the survival and favor myocardial hypertrophy in aged mice.

FONTANA ESTEVEZ F; SEROPIAN I; GONZALEZ G. ; LLAMOSAS MC; MIKSZTOWICZ V; BETAZZA C; MORALES C

Congreso; LXIV Reunión Anual de la Sociedad Argentina de Investigación Clínica; 2019

Abstract/Resumen: Galectin 3 (Gal-3), a ß-galactosidasebinding lectin widely expressed in the immune system, hasproinflammatory and profibrotic effects. Gal-3 participates inventricular remodeling (VR), hypertension, acute myocardialinfarction and heart failure. However, the role of Gal-3 onmortality and cardiac remodeling associated with aging has notbeen previously studied. We aimed to study if genetic deletion ofGal-3 modifies survival rate and VR associated with aging. Wildtype (WT, n= 54) and Gal-3 knockout (KO, n= 55) mice were inhoused and maintained on a 12 h light/dark cycle during 24months. Animals had access to water and food ad libitum. Waterand food consumption, body weight and survival rate werequantified. After 24 months of follow up, systolic blood pressurewas measured by plethysmography. Heart (HW), lungs (LW),kidneys (KW) and spleen (SW) were weight and tibia length (TL)measured. Student?s T tes t was used for comparison amonggroups and log rank test for survival curves (Kaplan meier).Results (Mean±SEM): Survival rate was significantly reduced inGal-3KO mice as compared with WT (p= 0.02). Water and foodconsumption was higher in Gal-3 KO mice: 5.5 ± 0.1ml/animal/week vs 3.3 ± 0.1 ml/animal/week (p