期刊
PHYSIOLOGICAL GENOMICS
卷 15, 期 1, 页码 65-74出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physiolgenomics.00181.2002
关键词
array; atherosclerosis; coronary artery disease/myocardial infarction; gene expression; sudden death
资金
- NHLBI NIH HHS [R01 HL066251-04, R01 HL066251-03, R01 HL066251-02, R01 HL066251-01A2, R01 HL065630-04, R01 HL065630-03, R01 HL065630-02, R01 HL065630-01] Funding Source: Medline
Genetic factors increase the risk to coronary artery disease ( CAD). To date, a limited number of genes that potentially contribute to development of CAD have been identified. In this study, we have performed large-scale gene expression analysis of similar to 12,000 human genes in nine severely atherosclerotic and six nonatherosclerotic human coronary arteries using oligonucleotide microarrays. Fifty-six genes showed differential expression in atherosclerotic coronary artery tissues; expression of 55 genes was increased in atherosclerotic coronary arteries, whereas only one gene, GST, encoding a reducing agent, showed downregulated expression. The expression data of selected genes were validated by quantitative RT-PCR analysis as well as immunostaining. The associations of 49 genes with CAD appear to be novel, and they include genes encoding ICAM-2, PIM-2, ECGF1, fusin, B cell activator (BL34, GOS8), Rho GTPase activating protein-4, retinoic acid receptor responder, beta2-arrestin, membrane aminopeptidase, cathepsins K and H, MIR-7, TNF-alpha-induced protein 2 (B94), and flavocytochrome 558. In conclusion, we have identified 56 genes whose expression is associated with CAD, and 49 of them may represent new genes linked to CAD.
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