Age-related cardiac remodeling and apoptosis are exacerbated in aged mice with genetic deletion of galectin 3.

FONTANA ESTEVEZ, FLORENCIA S.; BETAZZA, MARÍA CELESTE; SEROPIAN, IGNACIO; PENAS, FEDERICO; KOUYOUMDZIAN, NICOLÁS; SILVA, MG; SELSER, CAROLINA; VILLAVERDE, ALEJO; TOUCEDA, VANESSA; BUSTOS, ROMINA; VIDAL, MARÍA AGUSTINA; CIANCIULLI, TOMÁS; MEDINA, VANINA; CHOI, MARCELO; GIRONACCI, MARIELA; MIKSZTOWICZ, VERÓNICA; GONZÁLEZ, GERMÁN E.

Mar del Plata

Encuentro; LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; 2022

Sociedad Argentina de Investigación Clínica

Background: We showed that Galectin-3 deficiency (Gal3KO) exacerbated myocardial hypertrophy and fibrosis in aged mice. However, if Gal3KO increases myocardial apoptosis and alters renal function in mice with hypertrophic hearts and kidneys and with normal systolic blood pressure is still unknown. Objective: We aimed to continue investigating the age-associated physiological changes in Gal3KO mice to study if aged hearts exacerbate myocardial apoptosis, and if kidney hypertrophy is linked to renal dysfunction. Methods: Male C57 and Gal3KO mice were followed up for 24 months. After 2 years, animals were isolated in metabolic cages to recollect 24hs diuresisto quantified renal Creatinine and Albumin. After euthanasia, animal tissues were harvested, and cardiac apoptosis were quantified in Tunnel positive cells. With Radioimmunoassay cardiac levels of Angiotensin (Ang) II and Ang 1-7 were quantified. RT q-PCR was performed to quantified cardiac mRNA of TGF B, MMP 9 and Sirtuins 1 and 7 (SIRT). Results: (Media±SEM C57vsGal3KO). At 24 months, Gal3KO mice had exacerbated levels of cardiac Ang II (3±0.5 vs 7±1.5 ng/g, p