Cardiac-deleterious role of galectin-3 in chronic angiotensin II-induced hypertension

Document Type

Article

Publication Date

11-1-2016

Publication Title

American journal of physiology. Heart and circulatory physiology

Keywords

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

Abstract

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

PubMed ID

27496875

Volume

311

Issue

5

First Page

1287

Last Page

1287

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