title: Galectin-3 mediates aldosterone-induced vascular fibrosis.
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.
  
  
  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.
authors.affiliation: Inserm, U961, Faculty of Medicine, Université de Lorraine, Vandoeuvre-lès-Nancy, France.
authors.forename: Laurent
authors.initials: L
authors.lastname: Calvier
authors.forename: Maria
authors.initials: M
authors.lastname: Miana
authors.forename: Pascal
authors.initials: P
authors.lastname: Reboul
authors.forename: Victoria
authors.initials: V
authors.lastname: Cachofeiro
authors.forename: Ernesto
authors.initials: E
authors.lastname: Martinez-Martinez
authors.forename: Rudolf A
authors.initials: RA
authors.lastname: de Boer
authors.forename: Françoise
authors.initials: F
authors.lastname: Poirier
authors.forename: Patrick
authors.initials: P
authors.lastname: Lacolley
authors.forename: Faiez
authors.initials: F
authors.lastname: Zannad
authors.forename: Patrick
authors.initials: P
authors.lastname: Rossignol
authors.forename: Natalia
authors.initials: N
authors.lastname: López-Andrés
mesh_terms: D000450:Aldosterone; D000818:Animals; D001794:Blood Pressure; D002478:Cells, Cultured; D024042:Collagen Type I / Q000096:biosynthesis; D004195:Disease Models, Animal; D005355:Fibrosis; D037502:Galectin 3 / Q000037:antagonists & inhibitors / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D006973:Hypertension / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D007249:Inflammation / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D032389:Myocytes, Smooth Muscle / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D034622:RNA Interference; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014162:Transfection; D015854:Up-Regulation; D059289:Vascular Stiffness
chemical_list: D024042:Collagen Type I; D037502:Galectin 3; C485095:Lgals3 protein, mouse; D000451:Mineralocorticoid Receptor Antagonists; D000450:Aldosterone