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TARGET GENES IN MOUSE AORTA
1 Departments of Internal Medicine and Physiology & Biophysics, University of Iowa College of Medicine, Iowa City, IA, USA; Center for Bioinformatics and Computational Biology, University of Iowa College of Medicine, Iowa City, IA, USA
2 Departments of Internal Medicine and Physiology & Biophysics, University of Iowa College of Medicine, Iowa City, IA, USA
3 Center for Bioinformatics and Computational Biology, University of Iowa College of Medicine, Iowa City, IA, USA
* To whom correspondence should be addressed. E-mail: curt-sigmund{at}uiowa.edu.
Diminished activity of PPAR
may play a role in the pathogenesis of hypertension and vascular dysfunction. To better understand what genes are regulated by
PPAR, an experimental dataset was generated by microarray analysis, in duplicate, of pooled aortic mRNA isolated from mice treated for 21 days with a PPAR agonist (rosiglitazone) or vehicle. Of the 12488 probe sets present on the array (Affymetrix MG-U74Av2), 181 were differentially expressed between groups according to a statistical metric generated using Affymetrix software. A significant correlation was observed between the microarray results and real time RT-PCR analysis of 39 of these genes. Cluster analysis revealed 3 expression patterns, 29 transcripts of moderate abundance that were decreased
(-93%) to very low levels, 106 transcripts that were downregulated (-42%), and 46 transcripts that were upregulated (+70%). Functional groups that were decreased included inflammatory response (-93%, n=6), immune response (-86%, n=7), and cytokines (-82%, n=7). There was an overall upregulation in the oxidoreductase activity group (+47%, n=9). Individually, 6 transcripts in this group were increased (+72%) and 3 were decreased (-34%). 14 of the genes map to regions in the rat genome that have been linked to increased blood pressure and of 142 upstream regions analyzed, sequences resembling the DNA binding site for PPAR were identified in 101 of the differentially expressed genes.
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