title: Myocardial expression level of neural cell adhesion molecule correlates with reduced left ventricular function in human cardiomyopathy.
abstract: BACKGROUND
  Recently, we screened for cardiac genes induced by metabolic stress and identified neural cell adhesion molecule (NCAM) as a candidate. This study aimed to clarify the expression pattern of NCAM in human cardiomyopathy.
  
  
  RESULTS
  A total of 64 cardiac tissue samples of patients with dilated cardiomyopathy were dichotomized according to the immunohistochemically determined signal intensity of NCAM staining (NCAM-high and NCAM-low groups). Clinical and hemodynamic data of the patients were compared between the 2 groups. Fibrosis area, left ventricular end-diastolic volume index, and left ventricular diastolic pressure were greater in the NCAM-high group (22.8% versus 11.6%, P<0.05; 130.3±57.6 versus 104.8±31.7 mL/m(2), P<0.05; 14.3±8.0 versus 8.8±4.7 mm Hg, P<0.005; respectively). Incidence of cardiac death and admission for worsening heart failure was higher in the NCAM-high group during a follow-up of 6.3 years (log-rank P<0.05). Another 18 tissue samples were analyzed to determine the relationships between expression level of NCAM and major metabolic genes as well as hemodynamic parameters. The mRNA level of NCAM correlated with the serum (r=0.58; P=0.01) and mRNA levels (r=0.61; P=0.008) of brain-derived natriuretic peptides. It was also correlated with the mRNA levels of proliferator-activated receptor-γ coactivator-1 α (r=0.69; P=0.002) and the nuclear respiratory factor 1 (r=0.74; P<0.001).
  
  
  CONCLUSIONS
  Expression of NCAM was associated with worsening hemodynamic parameters and major metabolic genes. Together with our previous findings, these data support the involvement of NCAM in left ventricular remodeling, revealing new insights into the pathophysiology of heart failure.
authors.affiliation: Department of Cardiovascular Center, Osaka Red Cross Hospital, Osaka, Japan.
authors.forename: Kazuya
authors.initials: K
authors.lastname: Nagao
authors.forename: Naoya
authors.initials: N
authors.lastname: Sowa
authors.forename: Katsumi
authors.initials: K
authors.lastname: Inoue
authors.forename: Motoko
authors.initials: M
authors.lastname: Tokunaga
authors.forename: Kohei
authors.initials: K
authors.lastname: Fukuchi
authors.forename: Koji
authors.initials: K
authors.lastname: Uchiyama
authors.forename: Haruyasu
authors.initials: H
authors.lastname: Ito
authors.forename: Fujio
authors.initials: F
authors.lastname: Hayashi
authors.forename: Toshinori
authors.initials: T
authors.lastname: Makita
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Inada
authors.forename: Masaru
authors.initials: M
authors.lastname: Tanaka
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kimura
authors.forename: Koh
authors.initials: K
authors.lastname: Ono
mesh_terms: D001706:Biopsy; D006328:Cardiac Catheterization; D009202:Cardiomyopathies / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D019006:Neural Cell Adhesion Molecules / Q000096:biosynthesis / Q000235:genetics*; D012313:RNA / Q000235:genetics*; D060888:Real-Time Polymerase Chain Reaction; D012189:Retrospective Studies; D018487:Ventricular Dysfunction, Left / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D019006:Neural Cell Adhesion Molecules; D012313:RNA
keywords: cardiomyopathies; heart failure; neural cell adhesion molecule