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European Heart Journal Advance Access originally published online on March 26, 2009
European Heart Journal 2009 30(10):1229-1236; doi:10.1093/eurheartj/ehp088
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org

Increased systemic and myocardial expression of neutrophil gelatinase-associated lipocalin in clinical and experimental heart failure

Arne Yndestad1,2,*, Linn Landrø1, Thor Ueland1,3, Christen P. Dahl1,2, Trude H. Flo4, Leif Erik Vinge2,5, Terje Espevik4, Stig S. Frøland6, Cathrine Husberg2,7, Geir Christensen2,7, Kenneth Dickstein8, John Kjekshus9, Erik Øie1,2,9, Lars Gullestad2,9 and Pål Aukrust1,6

1 Research Institute for Internal Medicine, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway
2 Centre for Heart Failure Research, University of Oslo, Oslo, Norway
3 Department of Endocrinology, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway
4 Institute of Cancer Research and Molecular Biology, Norwegian University of Science and Technology, Trondheim, Norway
5 Institute for Surgical Research, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway
6 Section of Clinical Immunology and Infectious Diseases, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway
7 Institute for Experimental Medical Research, Ullevål University Hospital, University of Oslo, Oslo, Norway
8 Department of Cardiology, Stavanger University Hospital, Stavanger, Norway
9 Department of Cardiology, Rikshospitalet University Hospital, Oslo, Norway

Received 30 July 2008; revised 26 January 2009; accepted 18 February 2008; online publish-ahead-of-print 26 March 2009.

* Corresponding author. Tel: +47 23 07 36 29, Fax: +47 23 07 36 30, Email: arne.yndestad{at}medisin.uio.no

Aims: Neutrophil gelatinase-associated lipocalin (NGAL or lipocalin-2) is a glycoprotein with bacteriostatic properties. Growing evidence suggests that NGAL may also be involved in cell survival, inflammation, and matrix degradation. We therefore aimed to investigate the role of NGAL in heart failure (HF).

Methods and results: Our main findings were (i) patients with acute post-myocardial infarction (MI) HF (n = 236) and chronic HF (n = 150) had elevated serum levels of NGAL (determined by enzyme immunoassay), significantly correlated with clinical and neurohormonal deterioration, (ii) in patients with HF following acute MI, elevated NGAL levels of at baseline were associated with adverse outcomes (median of 27 months follow-up), (iii) in a rat model of post-MI HF, NGAL/lipocalin-2 gene expression was increased in the non-ischaemic part of the left ventricle primarily located to cardiomyocytes, (iv) strong NGAL immunostaining was found in cardiomyocytes within the failing myocardium both in experimental and clinical HF, (v) interleukin-1β and agonists for toll-like receptors 2 and 4, representing components of the innate immune system, were potent inducers of NGAL/lipocalin-2 in isolated neonatal cardiomyocytes.

Conclusion: Our demonstration of enhanced systemic and myocardial NGAL expression in clinical and experimental HF further support a role for innate immune responses in the pathogenesis of HF.

Key Words: Heart failure • Lipocalin • Innate immunity • Matrix metalloproteinase


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