Cardiac hypertrophy and mortality are increased in aged mice with genetic deletion of galectin 3

FLORENCIA S. FONTANA ESTEVEZ ; CELESTE BETAZZA; IGNACIO SEROPIAN; MARÍA AGUSTINA VIDAL

Congreso; REUNION ANUAL SAIC 2020; 2020

Aging is a physiological process associated with highly prevalent cardiovascular pathologies such as arterial hypertension, acute myocardial infarction and heart failure. We aimed to study if genetic deletion of Galectin 3 (Gal3), a β-galactosidase with proinflammatory and profibrotic effects, modifies survival rate, ventricular remodeling and systolic blood pressure (SBP) in aged mice. Wild type C57BL/6 (C57; n=54) and Gal3 knockout (Gal3KO; n=55) mice had access to water and food ad libitum for 24 months. Survival rate was quantified. After 2 years of follow up, SBP was measured by plethysmography. By echocardiography (ECO) in sedated mice, the wall thickness (mm) and left ventricular (LV) diameter were measured. Additionally; shortening fraction (SF, %) and cardiac mass (mm3) were calculated. Then, animals were euthanized, the organs harvested, weighted and the tibia length (TL) measured. Results (Mean ± SE): At 24 months, the survival rate was reduced in Gal3KO compared to C57 group (P=0.02). SBP (mmHg) was 112 ± 3 in C57 vs 114 ± 3 in Gal3KO (P=NS). SF (%) was 61 ± 1 C57 vs 60 ± 2 Gal3KO (P=NS). Posterior wall thickness (mm) was: 0.8 ± 0.02 in C57 vs 1.5 ± 0.2 in Gal3KO (P=0.0003) and 1 ± 0.02 in C57 vs 2 ± 0.1 in Gal3KO (P=0.0003) as measured in diastole and systole respectively, while anterior wall thickness (mm) in systole was 1 ± 0.02 in C57 vs 2 ± 0.1 in Gal3KO (P=0.,0005). Cardiac mass (mm3) was 80 ± 10 vs 140 ± 20 in C57 and Gal3KO mice respectively (P=0.01). Left ventricular end systolic and end diastolic diameter (mm) were 1 ± 0.1 in C57 vs 1 ± 0.1 in Gal3KO and 3 ± 0.1 in C57 vs 3 ± 0.1 in Gal3KO (P=NS). At necropsy: Heart weight/TL and kidney weight/TL were 8 ± 0.3 and 9 ± 0.3 (p