Myocardial hypertrophy, fibrosis and angiotensin II are exacerbated in aged mice with genetic mutation of Galectin 3

FONTANA ESTEVEZ, FLORENCIA S.; BETAZZA, MARÍA CELESTE; TOUCEDA, VANESSA; SILVA, MG; PENAS, FEDERICO; SEROPIAN, IGNACIO; SELSER, CAROLINA; VILLAVERDE, ALEJO; CIANCIULLI, TOMÁS; GIRONACCI, MARIELA; MIKSZTOWICZ, VERÓNICA; GONZÁLEZ, GERMÁN E.

Encuentro; Reunión Anual de la Sociedad Argentina de Fisiología (SAFIS); 2021

Sociedad Argentina de Fisiología

Background: Aging is a physiological process associated with highly prevalent cardiovascular pathologies such as arterial hypertension and heart failure. Galectin 3 (Gal3) is a β-galactosidase with proinflammatory and profibrotic effects associated with ventricular remodeling under acute pathological conditions. Objective: We aimed to study if genetic deletion of Gal3 (Gal3KO) modifies the aged related cardiovascular changes in old mice. Methods: Male C57 and Gal3KO mice were followed up for 24 months. After 2 years, non-invasive systolic blood pressure (SBP, mmHg) was measured and echocardiography was performed. Myocyte cross-sectional area (MCSA) and Interstitial fibrosis were quantified in H&E and Picrosirius red-stained sections. SIRT-7, MMP-2, and MMP-9 mRNA levels were measured by RT-qPCR. Cardiac Angiotensin II (ANGII) levels were quantified by radioimmunoassay. Results: (Media±SEM). At 24 months SBP was similar between groups: 116±4 in C57 vs 116±4 in Gal3KO (p=NS), and fractional shortening (%) also showed similar values 61±1 vs 60±4 (p=NS). Gal3KO mice had significantly increased cardiac hypertrophy measure by 1) cardiac mass (mg/mm) (9.7±1.3 vs 7.9±1.4, p