title: Adiponectin ameliorates endotoxin-induced acute cardiac injury.
abstract: BACKGROUND
  Obesity is a risk factor for cardiovascular disease. Increasing evidence suggests that reduced levels of the adipocyte-derived plasma protein adiponectin are associated with an increased cardiovascular risk. Here, we examined the effects of adiponectin on lipopolysaccharide- (LPS-) induced acute cardiac injury in vivo.
  
  
  RESULTS
  A single dose of LPS (10 mg/kg) was intraperitoneally injected into wild-type (WT) and adiponectin-knockout (APN-KO) mice. Following LPS administration, APN-KO mice had exacerbation of left ventricular (LV) systolic dysfunction compared with WT mice. Administration of LPS to WT and APN-KO mice led to an increased expression of inflammatory cytokines including TNF-α and IL-6 in the heart, but the magnitude of this induction was greater in APN-KO mice compared to WT mice. Systemic delivery of an adenoviral vector expressing adiponectin (Ad-APN) improved LPS-induced LV dysfunction in APN-KO mice, and this effect was accompanied by the reduced expression of TNF-α and IL-6 in the heart. Administration of etanercept, a soluble TNF receptor abolished the reduced LV contractile function in response to LPS in APN-KO mice.
  
  
  CONCLUSIONS
  These results suggest that adiponectin protects against LPS-induced acute cardiac injury by suppressing cardiac inflammatory responses, and could represent a potential therapeutic target in sepsis-associated myocardial dysfunction.
authors.affiliation: Department of Vascular Surgery, Cardiology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Watanabe
authors.affiliation: Department of Cardiology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa, Nagoya 466-8550, Japan.
authors.forename: Rei
authors.initials: R
authors.lastname: Shibata
authors.affiliation: Molecular Cardiovascular Medicine, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Ouchi
authors.affiliation: Department of Cardiology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa, Nagoya 466-8550, Japan.
authors.forename: Takahiro
authors.initials: T
authors.lastname: Kambara
authors.affiliation: Molecular Cardiovascular Medicine, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
authors.forename: Koji
authors.initials: K
authors.lastname: Ohashi
authors.affiliation: Department of Cardiology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa, Nagoya 466-8550, Japan.
authors.forename: Li
authors.initials: L
authors.lastname: Jie
authors.affiliation: Department of Cardiology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa, Nagoya 466-8550, Japan.
authors.forename: Yoko
authors.initials: Y
authors.lastname: Inoue
authors.affiliation: Department of Cardiology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa, Nagoya 466-8550, Japan.
authors.forename: Toyoaki
authors.initials: T
authors.lastname: Murohara
authors.affiliation: Department of Vascular Surgery, Cardiology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
authors.forename: Kimihiro
authors.initials: K
authors.lastname: Komori
mesh_terms: D052242:Adiponectin / Q000235:genetics / Q000276:immunology*; D000818:Animals; D016207:Cytokines / Q000276:immunology*; D006352:Heart Ventricles / Q000276:immunology*; D008070:Lipopolysaccharides; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009200:Myocardial Contraction / Q000276:immunology*; D009205:Myocarditis / Q000139:chemically induced / Q000276:immunology*; D018487:Ventricular Dysfunction, Left / Q000139:chemically induced / Q000276:immunology*
chemical_list: D052242:Adiponectin; D016207:Cytokines; D008070:Lipopolysaccharides