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Cardiovascular Research Advance Access originally published online on August 14, 2007
Cardiovascular Research 2008 77(2):425-431; doi:10.1093/cvr/cvm003
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

Mitochondrial uncoupling protein 2 mediates temperature heterogeneity in atherosclerotic plaques

Tim J.L. Van De Parre1, Wim Martinet1, Stefan Verheye2, Mark M. Kockx3, Glenn Van Langenhove2, Arnold G. Herman1 and Guido R.Y. De Meyer1,*

1 Division of Pharmacology, University of Antwerp, Universiteitsplein 1, B-2610 Wilrijk, Belgium
2 Antwerp Cardiovascular Institute, Middelheim Hospital, Antwerp, Belgium
3 Department of Pathology, Middelheim Hospital, Antwerp, Belgium

* Corresponding author. Tel: +32 3 820 27 37; fax: +32 3 820 25 67. E-mail address: guido.demeyer{at}ua.ac.be

Aims: Rupture-prone atherosclerotic plaques show an elevated temperature, but a molecular explanation for this phenomenon is unknown. Here, we investigated whether mitochondrial uncoupling protein 2 (UCP2) could be involved because this protein is a macrophage homologue of thermogenin in brown fat tissue.

Methods and results: Immunohistochemistry, western blotting, and real-time quantitative polymerase chain reaction were used to detect UCP2 expression in human and rabbit atherosclerotic plaques. Temperature was measured in plaques with thermography catheters and in cultured cells with precision thermometers. UCP2 was abundantly expressed in subendothelial macrophages of atherosclerotic plaques but not in deeper layers of the plaque. Ex vivo temperature measurements in atherosclerotic rabbit thoracic aorta demonstrated a correlation between local plaque temperature, total macrophage mass, and UCP2 expression. In vitro, chemical uncoupling of macrophages with sodium cyanide resulted in heat production ({Delta}T = 0.13 ± 0.04°C vs. controls). Also, overexpression of UCP2 in cultured cells led to a similar increase in temperature.

Conclusion: Our findings provide evidence that temperature heterogeneity in atherosclerotic plaques is at least in part attributed to UCP2 expression in macrophages. The heat generated might be used to detect unstable, macrophage-rich, atherosclerotic plaques via thermography.

KEYWORDS Atherosclerosis; Macrophages; Mitochondria

Time for primary review: 29 days


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