Changes in gene expression in atherosclerotic plaques analyzed using DNA array

Significant Expression of Endoglin (CD105), TGFβ-1 and TGFβ R-2 in the Atherosclerotic Aorta: An Immunohistological Study

“…Flk-1 is known as the major regulator of endothelial proliferation and vascular permeability in response to VEGF 29) . In fact, upregulation of the Flk-1 gene was detected in human atherosclerotic plaques using DNA array technology 17) . In the present study, we clearly observed the expression of Flk-1 and endoglin in atherosclerotic lesions of types through to , whereas non-atherosclerotic le- 16) , as they stated that VEGF could be one of the growth factors involved in the development of intraplaque microvessels in human coronary arteries.…”

“…Inoue et al 16) observed the expression of VEGF and its two receptors, flt-1 and Flk-1, in human coronary atherosclerosis. Furthermore, a study using DNA array technology showed up-regulation of the Flk-1 gene in human atherosclerotic plaques 17) . In the present study, we detected the expression of endoglin (CD105) with the TGF receptor complex system, as well as VEG-FR-2 (Flk-1), angiogenesis-related factors in human aortic atherosclerotic lesions, by immunohistochemistry.…”

Genome-Wide Expression Studies of Atherosclerosis

“…16,22 However, a detailed microscopic characterization of human samples has only been given in 2 studies. 18,28 Consequently, this lack of transparency in the morphology of analyzed samples hinders extrapolation and comparison of gene expression results. In only a minority of studies, 10,[25][26][27][28] the expression profiles of samples with a uniform cell content have been compared.…”

“…However, most of these studies aimed to identify the expression level of individual genes, and not pathways. 18 -20 In these studies, GO analysis suggested that the differentially expressed genes were involved in inflammation, 19,21,22 cell turnover, 19,21,22 matrix degradation, 18,19 lipid metabolism, 18,19 coding for matrix proteins, 20 or originated from SMC proliferation and dedifferentiation. 21 Thus, to date, gene expression studies have merely validated the differential expression of genes and pathways known to be involved in atherosclerosis, [42][43][44][45] and have yet to fully exploit the power and possibilities of identifying novel players (and eventually novel pathways) underlying atherosclerosis.…”

Catechol-O-methyltransferase promoter hypomethylation is associated with the risk of coronary heart disease

“…DNA methylation studies on CHD have primarily focused on genes related to estrogen receptors (ESR1 and ESR2), the immune system (FOXP3, PLA2G7 and MMP-9), lipid metabolism (ABCA1, KLF2 and LRP1), oxidative stress (GSTP1, BNIP3 and EC-COD), blood coagulation (TM and P2Y12) and genes on chromosome 9p21 (BAX, BCL-2 and TIMP3) (7). In addition, low promoter methylation was found to account for increased expression of the 15-lipoxygenase (ALOX15) gene (8). Furthermore, coagulation factor VII (F7) promoter hypomethylation has been correlated with higher plasma expression levels of activated coagulation factor VII (FVIIa), and has been shown to contribute towards an increased risk of CHD (9).…”