Van Eyk, Dunn - Proteomic and Genomic Analysis of Cardiovascular Disease - 2003 (522919), страница 44
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Cluster analysiswas used to further interpret the data. Vascular inflammation was mimicked bytreating human vascular SMC with tumor necrosis factor a (TNFa), and subsequent array analysis revealed the importance of eotaxin and its receptor in inflammatory cell recruitment [31]. Endothelial cell senescence was demonstrated usingcultured endothelial cells of early and late passages, and it was found that the expression of thymosin b-10 was decreased, which might contribute to the senescent phenotype by reducing the endothelial cell plasticity [32]. Wuttge et al. analyzed the gene expression during atherogenesis in apoE deficient mouse andfound that atherogenesis is not a linear process with a maximal expression at advanced lesions stage, instead the gene expression has its peaks at the intermediatelesion stage [33].
The gene expression profiles between aorta and vena cava werestudied in macaques, and 68 differentially expressed genes out of 4,048 genes hadelevated expression in aorta [34]. The expression patterns in fibrous cap versus adjacent media in human atherosclerotic lesions was studied by array of 588 clones,and the induction of Egr-1 expression was detected also in a mouse model [35].The expression differences between human stable and ruptured plaque was studied using suppression subtractive hybridization and macroarrays, and upregulatedexpression of periphilin, a phosphoprotein involved in process of lipolysis, in ruptured plaques was detected [36]. Human activated SMC expression was studied bydifferential display, and 10 known and 30 novel “smooth muscle activation-specific genes” were identified [37].Analysis of atherogenesis with genomics techniques is still in a very early stage.However, there is no doubt that DNA array techniques will become a valuable toolfor studying gene expression patterns in atherosclerosis and identifying novel candidate genes.
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