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This Article Full Text Full Text (PDF) Corrigendum All Versions of this Article: 38/3/233    most recent 90364.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Cappuzzello, C. Articles by Capogrossi, M. C. PubMed PubMed Citation Articles by Cappuzzello, C. Articles by Capogrossi, M. C.

Call For Papers: Comparative Genomics

Gene expression profiles in peripheral blood mononuclear cells of chronic heart failure patients

¹ Laboratorio di Patologia Vascolare, Istituto Dermopatico dell'Immacolata IRCCS, Rome
² Laboratorio di Biologia Vascolare e Terapia Genica, Centro Cardiologico Monzino-IRCCS, Milan
³ Laboratorio di Oncologia Molecolare, Bioinformatic Unit, Istituto Dermopatico dell'Immacolata-IRCCS, Rome
⁴ Institute of Cardiology, Catholic University, Ospedale Gemelli
⁵ Laboratorio di Analisi, Istituto Dermopatico dell'Immacolata-IRCCS, Rome, Italy

The present study was aimed at identifying chronic heart failure (CHF) biomarkers from peripheral blood mononuclear cells (PBMCs) in patients with ischemic (ICM) and nonischemic dilated (NIDCM) cardiomyopathy. PBMC gene expression profiling was performed by Affymetrix in two patient groups, 1) ICM (n = 12) and 2) NIDCM (n = 12) New York Heart Association (NYHA) III/IV CHF patients, vs. 3) age- and sex-matched control subjects (n = 12). Extracted RNAs were then pooled and hybridized to a total of 11 microarrays. Gene ontology (GO) analysis separated gene profiling into functional classes. Prediction analysis of microarrays (PAM) and significance analysis of microarrays (SAM) were utilized in order to identify a molecular signature. Candidate markers were validated by quantitative real-time polymerase chain reaction. We identified a gene expression profiling that distinguished between CHF patients and control subjects. Interestingly, among the set of genes constituting the signature, chemokine receptor (CCR2, CX₃CR1) and early growth response (EGR1, 2, 3) family members were found to be upregulated in CHF patients vs. control subjects and to be part of a gene network. Such findings were strengthened by the analysis of an additional 26 CHF patients (n = 14 ICM and n = 12 NIDCM), which yielded similar results. The present study represents the first large-scale gene expression analysis of CHF patient PBMCs that identified a molecular signature of CHF and putative biomarkers of CHF, i.e., chemokine receptor and EGR family members. Furthermore, EGR1 expression levels can discriminate between ICM and NIDCM CHF patients.

microarray; cardiomyopathy; leukocyte