Article Dans Une Revue Arteriosclerosis, Thrombosis, and Vascular Biology Année : 2013

Galectin-3 mediates aldosterone-induced vascular fibrosis.

Résumé

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.

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Dates et versions

hal-00812594 , version 1 (12-04-2013)

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Laurent Calvier, Maria Miana, Pascal Reboul, Victoria Cachofeiro, Ernesto Martinez-Martinez, et al.. Galectin-3 mediates aldosterone-induced vascular fibrosis.. Arteriosclerosis, Thrombosis, and Vascular Biology, 2013, 33 (1), pp.67-75. ⟨10.1161/ATVBAHA.112.300569⟩. ⟨hal-00812594⟩
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