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Galectin-3 mediates aldosterone-induced vascular fibrosis.

By Laurent Calvier, Maria Miana, Pascal Reboul, Victoria Cachofeiro, Ernesto Martinez-Martinez, Rudolf A De Boer, Françoise Poirier, Patrick Lacolley, Faiez Zannad, Patrick Rossignol and Natalia López-Andrés


International audienceOBJECTIVE: Aldosterone (Aldo) is involved in arterial stiffness and heart failure, but the mechanisms have remained unclear. Galectin-3 (Gal-3), a β-galactoside-binding lectin, plays an important role in inflammation, fibrosis, and heart failure. We investigated here whether Gal-3 is involved in Aldo-induced vascular fibrosis. METHODS AND RESULTS: In rat vascular smooth muscle cells Gal-3 overexpression enhanced specifically collagen type I synthesis. Moreover Gal-3 inhibition by modified citrus pectin or small interfering RNA blocked Aldo-induced collagen type I synthesis. Rats were treated with Aldo-salt combined with spironolactone or modified citrus pectin for 3 weeks. Hypertensive Aldo-treated rats presented vascular hypertrophy, inflammation, fibrosis, and increased aortic Gal-3 expression. Spironolactone or modified citrus pectin treatment reversed all the above effects. Wild-type and Gal-3 knock-out mice were treated with Aldo for 6 hours or 3 weeks. Aldo increased aortic Gal-3 expression, inflammation, and collagen type I in wild-type mice at both the short- and the long-term, whereas no changes occurred in Gal-3 knock-out mice. CONCLUSIONS: Our data indicate that Gal-3 is required for inflammatory and fibrotic responses to Aldo in vascular smooth muscle cells in vitro and in vivo, suggesting a key role for Gal-3 in vascular fibrosis

Topics: aldosterone, collagen type I, fibrosis, galectin-3, vascular smooth muscle cells, MESH : Aldosterone, MESH : Animals, MESH : Male, MESH : Mice, MESH : RNA Interference, MESH : Mice, Inbred C57BL, MESH : Mice, Knockout, MESH : Mineralocorticoid Receptor Antagonists, MESH : Muscle, Smooth, Vascular, MESH : Myocytes, Smooth Muscle, MESH : Rats, MESH : Blood Pressure, MESH : Cells, Cultured, MESH : Rats, Wistar, MESH : Time Factors, MESH : Transfection, MESH : Up-Regulation, MESH : Vascular Stiffness, MESH : Collagen Type I, MESH : Inflammation, MESH : Disease Models, Animal, MESH : Fibrosis, MESH : Galectin 3, MESH : Humans, MESH : Hypertension, [ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/Hematology, [ SDV.BC ] Life Sciences [q-bio]/Cellular Biology, [ SDV.BBM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology
Publisher: American Heart Association
Year: 2013
DOI identifier: 10.1161/ATVBAHA.112.300569
OAI identifier: oai:HAL:hal-00812594v1
Provided by: Hal-Diderot
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