Galectin-3 mediates aldosterone-induced vascular fibrosis

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

Research output: Contribution to journalArticlepeer-review

290 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)67-75
Number of pages9
JournalArteriosclerosis, thrombosis, and vascular biology
Volume33
Issue number1
DOIs
StatePublished - Jan 2013
Externally publishedYes

Keywords

  • aldosterone
  • collagen type I
  • fibrosis
  • galectin-3
  • vascular smooth muscle cells

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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