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European Journal of Heart Failure 2008 10(1):30-38; doi:10.1016/j.ejheart.2007.11.005
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© 2008 European Society of Cardiology

Up-regulation of PPAR{gamma} in myocardial infarction

Daniela Fliegnera, Dirk Westermannb, Alexander Riadb, Carola Schuberta, Eva Bechera, Jens Fielitza, Carsten Tschöpeb and Vera Regitz-Zagroseka,c,*

a Cardiovascular Disease in Women, Charité, Center for Cardiovascular Research (CCR), Charité, University of Medicine Berlin Germany
b Department of Cardiology and Pneumology, University Hospital Benjamin Franklin, Free University of Berlin Germany
c German Heart Institute Berlin (DHZB) Germany

* Corresponding author. CCR — Center for Cardiovascular Research, Hessische Str. 3-4, 10115 Berlin, Germany. Tel.: +4930 450 525 172; fax: +4930 450 525 972. E-mail address: vera.regitz-zagrosek{at}charite.de (V. Regitz-Zagrosek)


  Abstract

Background: Peroxisome proliferator activated receptors (PPARs) are key regulators for cardiac energy metabolism after myocardial injury. We hypothesized, that PPARs are regulated in myocardial infarction (MI) and their activity is modulated by angiotensin receptor blockers (ARBs).

Methods: Following induction of MI, male rats were treated with placebo or the ARB irbesartan for three weeks. PPAR{alpha}, β/{delta} and {gamma} protein expression and gene expression of PPAR target genes and glucose transporters were measured. PPAR{gamma}-protein expression was analyzed by immunofluorescence.

Results: MI decreased LVP and dp/dtmax and increased LVEDP, this effect was counteracted by irbesartan. PPAR{alpha} and PPARβ/{delta} protein expression was not altered in MI and was not affected by irbesartan. PPAR{gamma} protein content was increased in the infarcted area and localized to cardiac myocytes and fibroblasts. In parallel, expression of CTGF was increased 10-fold in the infarcted zone. PPAR target genes (CD36, MCAD, ACO and GLUT4) were significantly decreased in infarcted tissue, and this was unaffected by irbesartan. However, CD36 and ACO in the non-infarcted areas were up-regulated by irbesartan.

Conclusion: Endogenous up-regulation of PPAR{gamma} in MI is insufficient to counteract the decrease in metabolic genes, but parallels an increase in the profibrotic mediator CTGF. Irbesartan increases fatty acid oxidating enzymes after MI independent of PPAR{gamma} regulation.

Key Words: Myocardial infarction • PPARs • Myocardial metabolism • Angiotensin receptor blockers (ARBs) • Fibrosis

Received July 5, 2007; Revised October 1, 2007; Accepted November 13, 2007


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