on November 18, 2004
Published online before print November 18, 2004, doi: 10.1161/01.ATV.0000151372.86863.a5
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Submitted on May 10, 2004
Accepted on November 11, 2004
Mouse Strain-Specific Differences in Vascular Wall Gene Expression and Their Relationship to Vascular Disease
Raymond Tabibiazar *;
From the Donald W. Reynolds Cardiovascular Clinical Research Center, Division of Cardiovascular Medicine (R. Tabibiazar, R.A.W., J.M.S., E.A.A., P.S.T., T.Q.), Department of Health Research and Policy (B.N., B.E., R. Tibshirani), and the Department of Statistics (B.E., R. Tibshirani), Stanford University School of Medicine, Stanford, Calif; and the Genome Sciences Department (E.M.R.), Lawrence Berkeley National Laboratory, Berkeley, Calif.
* To whom correspondence should be addressed. E-mail: rtabibiazar{at}cvmed.stanford.edu.
Objective--Different strains of inbred mice exhibit different susceptibility to the development of atherosclerosis. The C3H/HeJ and C57Bl/6 mice have been used in several studies aimed at understanding the genetic basis of atherosclerosis. Under controlled environmental conditions, variations in susceptibility to atherosclerosis reflect differences in genetic makeup, and these differences must be reflected in gene expression patterns that are temporally related to the development of disease. In this study, we sought to identify the genetic pathways that are differentially activated in the aortas of these mice.
Methods and Results--We performed genome-wide transcriptional profiling of aortas from C3H/HeJ and C57Bl/6 mice. Differences in gene expression were identified at baseline as well as during normal aging and longitudinal exposure to high-fat diet. The significance of these genes to the development of atherosclerosis was evaluated by observing their temporal pattern of expression in the well-studied apolipoprotein E model of atherosclerosis.
Conclusion--Gene expression differences between the 2 strains suggest that aortas of C57Bl/6 mice have a higher genetic propensity to develop inflammation in response to appropriate atherogenic stimuli. This study expands the repertoire of factors in known disease-related signaling pathways and identifies novel candidate genes for future study.
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