title: Lipocalin-2/neutrophil gelatinase-B associated lipocalin is strongly induced in hearts of rats with autoimmune myocarditis and in human myocarditis.
abstract: BACKGROUND
  Lipocalin-2/neutrophil gelatinase-B associated lipocalin (Lcn2/NGAL) is involved in the transport of iron and seems to play an important role in inflammation. A recent study has reported that it is also expressed in the failing heart and may be a biomarker not only for renal failure but also for heart failure. Because Lcn2/NGAL is thought to be induced by interleukin-1, it might be strongly induced in the presence of myocarditis.
  
  
  RESULTS
  This study investigated the expression of Lcn2/NGAL in rat experimental autoimmune myocarditis (EAM) and in human myocarditis. In EAM hearts, the expression of Lcn2/NGAL was markedly increased (>100-fold at an early stage), and in human myocarditis it was also highly expressed compared with non-inflammatory failing hearts. Lcn2/NGAL expressing cells in hearts with EAM and human myocarditis were identified as cardiomyocytes, vascular wall cells, fibroblasts and neutrophils. Lcn2/NGAL in EAM rats was also expressed in the liver. Plasma Lcn2/NGAL levels abruptly increased at an early stage of EAM, and high levels were initially sustained during the inflammatory stage, then decreased with recovery. In contrast, levels of B-type natriuretic peptide increased only slowly as the disease progressed.
  
  
  CONCLUSIONS
  Cardiomyocytes, vascular wall cells and fibroblasts in myocarditis strongly express Lcn2/NGAL via proinflammatory cytokines.
authors.affiliation: Division of Cardiology, Niigata University Graduate School of Medical and Dental Sciences, Japan
authors.forename: Limin
authors.initials: L
authors.lastname: Ding
authors.forename: Haruo
authors.initials: H
authors.lastname: Hanawa
authors.forename: Yoshimi
authors.initials: Y
authors.lastname: Ota
authors.forename: Go
authors.initials: G
authors.lastname: Hasegawa
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Hao
authors.forename: Fuyuki
authors.initials: F
authors.lastname: Asami
authors.forename: Ritsuo
authors.initials: R
authors.lastname: Watanabe
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Yoshida
authors.forename: Ken
authors.initials: K
authors.lastname: Toba
authors.forename: Kaori
authors.initials: K
authors.lastname: Yoshida
authors.forename: Minako
authors.initials: M
authors.lastname: Ogura
authors.forename: Makoto
authors.initials: M
authors.lastname: Kodama
authors.forename: Yoshifusa
authors.initials: Y
authors.lastname: Aizawa
mesh_terms: D000209:Acute-Phase Proteins / Q000235:genetics* / Q000378:metabolism; D000368:Aged; D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology / Q000503:physiopathology*; D004195:Disease Models, Animal; D005260:Female; D005347:Fibroblasts / Q000502:physiology; D015870:Gene Expression / Q000502:physiology; D006333:Heart Failure / Q000276:immunology / Q000503:physiopathology*; D006801:Humans; D007114:Immunization; D053583:Interleukin-1beta / Q000097:blood / Q000235:genetics; D000071068:Lipocalin-2; D054834:Lipocalins / Q000097:blood / Q000235:genetics* / Q000378:metabolism; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D008875:Middle Aged; D009205:Myocarditis / Q000276:immunology / Q000503:physiopathology*; D032383:Myocytes, Cardiac / Q000502:physiology; D009218:Myosins / Q000276:immunology; D020097:Natriuretic Peptide, Brain / Q000097:blood; D011518:Proto-Oncogene Proteins / Q000235:genetics* / Q000378:metabolism; D051381:Rats; D013552:Swine; D055815:Young Adult
chemical_list: D000209:Acute-Phase Proteins; D053583:Interleukin-1beta; C489506:LCN2 protein, human; C097278:Lcn2 protein, rat; D000071068:Lipocalin-2; D054834:Lipocalins; D011518:Proto-Oncogene Proteins; C495963:natriuretic peptide precursor type B, rat; D020097:Natriuretic Peptide, Brain; D020780:Matrix Metalloproteinase 9; D009218:Myosins