HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

Physiol. Genomics 18: 33-42, 2004. First published March 30, 2004; doi:10.1152/physiolgenomics.00027.2004
1094-8341/04 $5.00

This Article Free upon publication Full Text Full Text (PDF) Supplemental Tables & Figures All Versions of this Article: 18/1/33    most recent 00027.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Keen, H. L. Articles by Sigmund, C. D. Search for Related Content PubMed PubMed Citation Articles by Keen, H. L. Articles by Sigmund, C. D.

Gene expression profiling of potential PPAR target genes in mouse aorta

¹ Departments of Internal Medicine and Physiology and Biophysics, University of Iowa College of Medicine, Iowa City, Iowa 52242
² Center for Bioinformatics and Computational Biology, University of Iowa College of Medicine, Iowa City, Iowa 52242

Diminished activity of peroxisome proliferator-activated receptor- (PPAR) may play a role in the pathogenesis of hypertension and vascular dysfunction. To better understand what genes are regulated by PPAR, an experimental data set 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 12,488 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, six transcripts in this group were increased (+72%), and three were decreased (–34%). Fourteen 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.

gene expression analysis; bioinformatics; vasculature; mouse; transcription factor

This article has been cited by other articles:

				J. D. Miller, Y. Chu, R. M. Brooks, W. E. Richenbacher, R. Pena-Silva, and D. D. Heistad Dysregulation of Antioxidant Mechanisms Contributes to Increased Oxidative Stress in Calcific Aortic Valvular Stenosis in Humans J. Am. Coll. Cardiol., September 2, 2008; 52(10): 843 - 850. [Abstract] [Full Text] [PDF]

				C. C. Zhou, S. Ahmad, T. Mi, L. Xia, S. Abbasi, P. W. Hewett, C. Sun, A. Ahmed, R. E. Kellems, and Y. Xia Angiotensin II Induces Soluble fms-Like Tyrosine Kinase-1 Release via Calcineurin Signaling Pathway in Pregnancy Circ. Res., January 5, 2007; 100(1): 88 - 95. [Abstract] [Full Text] [PDF]

				D. G. Lemay and D. H. Hwang Genome-wide identification of peroxisome proliferator response elements using integrated computational genomics J. Lipid Res., July 1, 2006; 47(7): 1583 - 1587. [Abstract] [Full Text] [PDF]

				K. E. Knoll, J. L. Pietrusz, and M. Liang Tissue-specific transcriptome responses in rats with early streptozotocin-induced diabetes Physiol Genomics, April 14, 2005; 21(2): 222 - 229. [Abstract] [Full Text] [PDF]