title: Identification of a common gene expression signature in dilated cardiomyopathy across independent microarray studies.
abstract: OBJECTIVE
  This study was designed to identify a common gene expression signature in dilated cardiomyopathy (DCM) across different microarray studies.
  
  
  BACKGROUND
  Dilated cardiomyopathy is a common cause of heart failure in Western countries. Although gene expression arrays have emerged as a powerful tool for delineating complex disease patterns, differences in platform technology, tissue heterogeneity, and small sample sizes obscure the underlying pathophysiologic events and hamper a comprehensive interpretation of different microarray studies in heart failure.
  
  
  METHODS
  We accounted for tissue heterogeneity and technical aspects by performing 2 genome-wide expression studies based on cDNA and short-oligonucleotide microarray platforms which comprised independent septal and left ventricular tissue samples from nonfailing (NF) (n = 20) and DCM (n = 20) hearts.
  
  
  RESULTS
  Concordant results emerged for major gene ontology classes between cDNA and oligonucleotide microarrays. Notably, immune response processes displayed the most pronounced down-regulation on both microarray types, linking this functional gene class to the pathogenesis of end-stage DCM. Furthermore, a robust set of 27 genes was identified that classified DCM and NF samples with >90% accuracy in a total of 108 myocardial samples from our cDNA and oligonucleotide microarray studies as well as 2 publicly available datasets.
  
  
  CONCLUSIONS
  For the first time, independent microarray datasets pointed to significant involvement of immune response processes in end-stage DCM. Moreover, based on 4 independent microarray datasets, we present a robust gene expression signature of DCM, encouraging future prospective studies for the implementation of disease biomarkers in the management of patients with heart failure.
authors.affiliation: Department of Medicine I, University Hospital Grosshadern, Munich, Germany. andreas.barth@med.uni-muenchen.de
authors.forename: Andreas S
authors.initials: AS
authors.lastname: Barth
authors.forename: Ruprecht
authors.initials: R
authors.lastname: Kuner
authors.forename: Andreas
authors.initials: A
authors.lastname: Buness
authors.forename: Markus
authors.initials: M
authors.lastname: Ruschhaupt
authors.forename: Sylvia
authors.initials: S
authors.lastname: Merk
authors.forename: Ludwig
authors.initials: L
authors.lastname: Zwermann
authors.forename: Stefan
authors.initials: S
authors.lastname: Kääb
authors.forename: Eckart
authors.initials: E
authors.lastname: Kreuzer
authors.forename: Gerhard
authors.initials: G
authors.lastname: Steinbeck
authors.forename: Ulrich
authors.initials: U
authors.lastname: Mansmann
authors.forename: Annemarie
authors.initials: A
authors.lastname: Poustka
authors.forename: Michael
authors.initials: M
authors.lastname: Nabauer
authors.forename: Holger
authors.initials: H
authors.lastname: Sültmann
mesh_terms: D000917:Antibody Formation / Q000235:genetics; D002311:Cardiomyopathy, Dilated / Q000235:genetics* / Q000503:physiopathology; D018450:Disease Progression; D015536:Down-Regulation; D015870:Gene Expression; D020869:Gene Expression Profiling; D006801:Humans; D020411:Oligonucleotide Array Sequence Analysis