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Arterioscler Thromb Vasc Biol. 2013 Jan;33(1):67-75. doi: 10.1161/ATVBAHA.112.300569. Epub 2012 Nov 1.

Galectin-3 mediates aldosterone-induced vascular fibrosis.

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1
Inserm, U961, Faculty of Medicine, Université de Lorraine, Vandoeuvre-lès-Nancy, France.

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.

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.

PMID:
23117656
DOI:
10.1161/ATVBAHA.112.300569
[Indexed for MEDLINE]
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