The genetic mutation of Galectin 3 modified the aging process in mice.

FLORENCIA SOFÍA FONTANA ESTEVEZ; IGNACIO SEROPIAN; CELINA MORALES; CELESTE BETAZZA; VERONICA MIKSZTOWICZ; CLARA LLAMOSAS; GERMÁN E. GONZÁLEZ

Mar del Plata

Congreso; Reunión Anual SAIC - SAFE - SAB - SAP 2019; 2019

Galectin 3(GAL3) is a ß-galactosidase binding lectin widely express in the immune system. GAL3 has proinflammatory and profibrotic effects, it increases during ventricular remodeling(VR) associated with arterial hypertension and in patients with heart failure. The role of GAL3 on VR associated with aging was not studied yet. The aim of this investigation was to study if the genetic lack of GAL3 modifies mortality and the natural evolution of VR associated with aging. C57(n=54) and GAL3KO(n=55) mice  were  housed  in groups during 24 months,  they had access to water and food ad libitum and maintained on a 12-h light/dark cycle. We quantified: 1) Water and food consumption; 2)Body weight and 3) Survival rate. Mice  were euthanized; heart(HW), lungs(LW), kidneys(KW) and spleen(SW) were removed and weight for analysed. Tibia length(TL) was also measured. Results (Mean ± SEM): Survival rate was less in GAL3KO group vs C57 (P=0,02). Water consumption (ml/N) was significantly higher in GAL3KO group (5.5 ± 0.11) vs C57 (3.3 ± 0.07) (P