Genetic deletion of Galectin 3 reduced survival and favored myocardial hypertrophy in aged mice

FLORENCIA S. FONTANA ESTEVEZ, CELESTE BETAZZA, MARÍA CLARA LLAMOSAS, IGNACIO SEROPIAN, CELINA MORALES, VERÓNICA MIKSZTOWICZ, GERMÁN E. GONZÁLEZ

Mar del Plata

Congreso; Reunion anual de la Sociedad Argentina de Investigacion Clinica; 2019

S A I C . S A F E . S A B . SAP

Galectin 3 (Gal-3), a β-galactosidase binding lectin widely expressed in the immune system, has proinflammatory and profibrotic effects. Gal-3 participates in ventricular remodeling (VR), hypertension, acute myocardial infarction and heart failure. However, the role of Gal-3 on mortality and cardiac remodeling associated with aging has not been previously studied. We aimed to study if genetic deletion of Gal-3 modifies survival rate and VR associated with aging. Wild type (WT, n=54) and Gal-3 knockout (KO, n=55) mice were in-housed and maintained on a 12-h light/dark cycle during 24 months. Animals had access to water and food ad libitum. Water and food consumption, body weight and survival rate were quantified. After 24 months of follow up, systolic blood pressure was 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 among groups and log rank test for survival curves (Kaplan meier). Results (Mean±SEM): Survival rate was significantly reduced in Gal-3KO mice as compared with WT (P= 0.02). Water and food consumption was higher in Gal-3 KO mice: 5.5±0.1 ml/animal/week vs 3.3±0.1 ml/animal/week (P