Galectin-3 Mediates Aldosterone-Induced Vascular Fibrosis

Author:

Calvier Laurent1,Miana Maria1,Reboul Pascal1,Cachofeiro Victoria1,Martinez-Martinez Ernesto1,de Boer Rudolf A.1,Poirier Françoise1,Lacolley Patrick1,Zannad Faiez1,Rossignol Patrick1,López-Andrés Natalia1

Affiliation:

1. From the INSERM, Université de Lorraine UMR 961 (L.C., P.L., F.Z., P.R., N.L-A.), Vandoeuvre-Lès-Nancy, F-54500, France; Universidad complutense de Madrid (M.M., V.C., E.M-M.), Madrid, Spain; CNRS, Université de Lorraine UMR 7561 (P.R.), Vandoeuvre-Lès-Nancy, F-54500, France; Department of Cardiology, University Medical Center Groningen, University of Groningen (d.B.R.A), Groningen, The Netherlands; CNRS, Paris-Diderot University, UMR 7592 (F.P.), Paris, F-75000, France; CHU Nancy, Inserm Clinical...

Abstract

Objective— 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. Conclusion— 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.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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