title: Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction.
abstract: Galectin-1 (Gal-1), an evolutionarily conserved β-galactoside-binding lectin, plays essential roles in the control of inflammation and neovascularization. Although identified as a major component of the contractile apparatus of cardiomyocytes, the potential role of Gal-1 in modulating heart pathophysiology is uncertain. Here, we aimed to characterize Gal-1 expression and function in the infarcted heart. Expression of Gal-1 was substantially increased in the mouse heart 7 days after acute myocardial infarction (AMI) and in hearts from patients with end-stage chronic heart failure. This lectin was localized mainly in cardiomyocytes and inflammatory infiltrates in peri-infarct areas, but not in remote areas. Both simulated hypoxia and proinflammatory cytokines selectively up-regulated Gal-1 expression in mouse cardiomyocytes, whereas anti-inflammatory cytokines inhibited expression of this lectin or had no considerable effect. Compared with their wild-type counterpart, Gal-1-deficient (Lgals1(-/-)) mice showed enhanced cardiac inflammation, characterized by increased numbers of macrophages, natural killer cells, and total T cells, but reduced frequency of regulatory T cells, leading to impaired cardiac function at baseline and impaired ventricular remodeling 7 days after nonreperfused AMI. Treatment of mice with recombinant Gal-1 attenuated cardiac damage in reperfused AMI. Taken together, our results indicate a protective role for Gal-1 in normal cardiac homeostasis and postinfarction remodeling by preventing cardiac inflammation. Thus, Gal-1 treatment represents a potential novel strategy to attenuate heart failure in AMI.
authors.affiliation: VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, Virginia 23298-0281, USA.
authors.forename: Ignacio M
authors.initials: IM
authors.lastname: Seropian
authors.forename: Juan P
authors.initials: JP
authors.lastname: Cerliani
authors.forename: Stefano
authors.initials: S
authors.lastname: Toldo
authors.forename: Benjamín W
authors.initials: BW
authors.lastname: Van Tassell
authors.forename: Juan M
authors.initials: JM
authors.lastname: Ilarregui
authors.forename: Germán E
authors.initials: GE
authors.lastname: González
authors.forename: Mirian
authors.initials: M
authors.lastname: Matoso
authors.forename: Fadi N
authors.initials: FN
authors.lastname: Salloum
authors.forename: Ryan
authors.initials: R
authors.lastname: Melchior
authors.forename: Ricardo J
authors.initials: RJ
authors.lastname: Gelpi
authors.forename: Juan C
authors.initials: JC
authors.lastname: Stupirski
authors.forename: Alejandro
authors.initials: A
authors.lastname: Benatar
authors.forename: Karina A
authors.initials: KA
authors.lastname: Gómez
authors.forename: Celina
authors.initials: C
authors.lastname: Morales
authors.forename: Antonio
authors.initials: A
authors.lastname: Abbate
authors.forename: Gabriel A
authors.initials: GA
authors.lastname: Rabinovich
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D015687:Cell Hypoxia / Q000502:physiology; D002478:Cells, Cultured; D016207:Cytokines / Q000494:pharmacology; D005260:Female; D037483:Galectin 1 / Q000096:biosynthesis / Q000494:pharmacology / Q000502:physiology* / Q000627:therapeutic use; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D018836:Inflammation Mediators / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D009205:Myocarditis / Q000209:etiology / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism; D011994:Recombinant Proteins / Q000627:therapeutic use; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology*; D055815:Young Adult
chemical_list: D016207:Cytokines; D037483:Galectin 1; D018836:Inflammation Mediators; D011994:Recombinant Proteins