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Articles in PresS, published online ahead of print August 20, 2002
Physiol Genomics, 10.1152/physiolgenomics.00062.2002
Submitted on May 24, 2002
Accepted on August 19, 2002
B-mediated genes and down-regulation of PPARs in apoE-KO mice
1 Department of Internal Medicine, University of California, School of Medicine, Davis, CA, USA
2 Department of Pharmacology, Berlex Biosciences, Richmond, CA, USA
3 Department of Pathology, University of California, School of Medicine, Davis, CA, USA
4 Department of Cardiovascular Research, Berlex Biosciences, Richmond, CA, USA
* To whom correspondence should be addressed. E-mail: dmtham{at}ucdavis.edu.
Angiotensin II (Ang II) promotes vascular inflammation through nuclear factor-kappa B (NF-
B)-mediated induction of pro-inflammatory genes. The role of peroxisome proliferator-activated receptors (PPARs) in modulating vascular inflammation and atherosclersosis in vivo is unclear. The aim of the present study was to examine the effects of Ang II on PPARs and NF-B-dependent pro-inflammatory genes in the vascular wall in an in vivo model of atherosclerosis and aneurysm formation. Six-month old male apolipoprotein E-deficient (apoE-KO) mice were treated with Ang II (1.44 mg/kg per day for 30 days). Ang II enhanced vascular inflammation, accelerated atherosclerosis and induced formation of abdominal aortic aneurysms. These effects of Ang II in the aorta were associated with down-regulation of both PPAR-
and PPAR-
mRNA and protein, and an increase in transcription of monocyte chemotactic protein-1 (MCP-1), macrophage-colony stimulating factor (M-CSF), endothelial-selectin (E-selectin), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) throughout the entire aorta. Ang II also activated NF-B with increases in both p52 and p65 NF-B subunits. In summary, these in vivo results indicate that Ang II, through activation of NF-B-mediated pro-inflammatory genes, promotes vascular inflammation, leading to acceleration of atherosclerosis and induction of aneurysm in apoE-KO mice. Down-regulation of PPAR- and - by Ang II may diminish the anti-inflammatory potential of PPARs, thus contributing to enhanced vascular inflammation.
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