Cardiac-deleterious role of galectin-3 in chronic angiotensin II-induced hypertension.
Gonzalez GE, Rhaleb NE, D'Ambrosio MA, Nakagawa P, Liao TD, Peterson EL, Leung P, Dai X, Janic B, Liu YH, Yang XP, Carretero OA. Cardiac-deleterious role of Galectin-3 in Angiotension II-induced Hypertension. Am J Physiol Heart Circ Physiol. 2016 ;311(5):H1287-H1296.
American journal of physiology. Heart and circulatory physiology
Galectin-3 (Gal-3), a member of the β-galactoside lectin family, has an important role in immune regulation. In hypertensive rats and heart failure patients, Gal-3 is considered a marker for an unfavorable prognosis. Nevertheless, the role and mechanism of Gal-3 action in hypertension-induced target organ damage are unknown. We hypothesized that, in angiotensin II (ANG II)-induced hypertension, genetic deletion of Gal-3 prevents left ventricular (LV) adverse remodeling and LV dysfunction by reducing the innate immune responses and myocardial fibrosis. To induce hypertension, male C57BL/6J and Gal-3 knockout (KO) mice were infused with ANG II (3 μg·min
Medical Subject Headings
Angiotensin II; Animals; Antigens, CD; Antigens, Differentiation, Myelomonocytic; Blood Pressure; Blotting, Western; Cardiomegaly; Cytokines; Disease Models, Animal; Echocardiography; Enzyme-Linked Immunosorbent Assay; Fibrosis; Flow Cytometry; Galectin 3; Hypertension; Intercellular Adhesion Molecule-1; Macrophages; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Myocardium; Plethysmography; T-Lymphocytes, Regulatory; Vascular Cell Adhesion Molecule-1; Ventricular Dysfunction, Left; Ventricular Function, Left