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Cardiovascular Research 2002 54(1):175-182; doi:10.1016/S0008-6363(02)00238-9
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Increased gene expression of tumor necrosis factor superfamily ligands in peripheral blood mononuclear cells during chronic heart failure

Arne Yndestada,b,*, Jan Kristian Damåsa,b,c, Hans Geir Eikena,d, Torbjørn Holma,c, Terje Hauge, Svein Simonsenc, Stig S. Frølanda,b, Lars Gullestadf and Pål Aukrusta,b

aResearch Institute for Internal Medicine, Rikshospitalet University Hospital, University of Oslo, N-0027 Oslo, Norway
bSection of Clinical Immunology and Infectious Diseases, Rikshospitalet University Hospital, University of Oslo, N-0027 Oslo, Norway
cDepartment of Cardiology, Rikshospitalet University Hospital, University of Oslo, N-0027 Oslo, Norway
dMSD Cardiovascular Research Centre, Rikshospitalet University Hospital, University of Oslo, N-0027 Oslo, Norway
eCentre for Occupational and Environmental Medicine, Rikshospitalet University Hospital, University of Oslo, N-0027 Oslo, Norway
fDepartment of Medicine, Bærum Hospital, Sandvika, Norway

* Corresponding author. Tel.: +47-23-073-629; fax: +47-23-073-630 arne.yndestad{at}klinmed.uio.no

Objective: Inflammation may play a pathogenic role in chronic heart failure (CHF). The objective of the study was to characterise the imbalance in the cytokine network in CHF. Methods: cDNA expression arrays were used to analyse the gene expression of cytokines and related mediators in peripheral blood mononuclear cells (PBMC) from CHF patients (n=8) and healthy controls (n=8). Real-time quantitative reverse transcription–polymerase chain reaction (RT-PCR) was used to determine the gene expression of individual genes in additional 12 patients and eight controls. Results: From 375 genes, 34 were upregulated and two downregulated in CHF patients in the cDNA expression array experiments. Regulated genes included chemokines/-receptors, members of the transforming growth factor β superfamily, orphan receptors and in particular several members of the tumor necrosis factor (TNF) superfamily. Thus, 4-1BB ligand (L), APRIL, CD27L, CD40L, FasL, LIGHT, TRAIL-receptor 4 were upregulated, while TRAIL-receptor 3 was downregulated. Real-time quantitative RT-PCR confirmed significantly upregulated gene expression of APRIL, LIGHT, FasL and CD27L in CHF patients and showed in addition significantly enhanced gene expression of TNF{alpha} and TRAIL. Conclusion: The present study demonstrates differential gene expression in PBMC of several members of the cytokine network in CHF. In particular, the enhanced expression of several ligands in the TNF superfamily may reflect a potential pathogenic role of these cytokines in CHF.

KEYWORDS Heart failure; Immunology; Cytokines; Leukocytes; Gene expression


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