RESUMO
Objectives To explore the intrinsic factors related to the pathogenesis of acute arterial thrombosis (AAT) and to elucidate the patho-genesis of AAT on the basis of differentially expressed genes. Methods Patients with acute myocardial infarction (AMI), stable angina (SA) and healthy controls (n=20 per group) were recruited, and the whole human genome microarray analysis was performed to detect the dif-ferentially expressed genes among these subjects. Results Patients with AMI had disease-specific gene expression pattern. Biological func-tional analysis showed the function of T cells was significantly reduced, the mitochondrial metabolism significantly decreased, the ion me-tabolism was abnormal, the cell apoptosis and inflammatory reaction increased, the phagocytosis elevated, the neutrophil-mediated immunity increased and the post-traumatic repair of cells and tissues increased in AMI patients. The biological function in SA group and healthy con-trols remained stable and was comparable. Conclusions The reduced function of T cell gene models in AAT showed the dysfunction of the immune system. The pathogenesis of AAT may be related to the inflammatory reaction after arterial intima infection caused by potential pathogenic microorganisms.
RESUMO
Objective To investigate expression differences of neutrophil and mononuclear phagocyte related gene mRNAs among acute myocar-dial infarction (AMI), stable angina (SA) and control groups, and then discuss their expression characteristics in the stable angina pectoris (SAP) and AMI stages of coronary artery disease (CAD). Methods Whole Human Genome Oligo Microarrays were applied to assess the differential expression characteristics of neutrophil and mononuclear phagocyte related mRNAs in patients with AMI (n=20), SA (n=20) and controls (n=20). Results (1) Almost all colony-stimulating factors (CSF) and their receptors related mRNAs was up-regulated in AMI and SA groups compared with the control group, and the expression of granulocyte-macrophage colony stimulating factor receptor (GM-CSFR) and granulocyte colony stimulating factor receptor (G-CSFR) mRNAs in the AMI group was significantly up-regulated com-pared with the other two groups (P<0.01). (2) The expression of mRNAs related to monocyte chemoattractant protein-1 (MCP-1), CCR2 (MCP-1 receptor) and CXCR2 (IL-8 receptor) was significantly up-regulated (P<0.01) in AMI group compared with SA and control groups. IL-8 mRNA expression in the AMI group was clearly higher than the controls (P<0.05). (3) All mRNAs expression related to opsonic re-ceptors (IgG FcR and C3bR/C4bR) was significantly up-regulated in AMI group compared with SA and control group (P<0.01), and the SA group showed an upward trend compared with controls. (4) Most pattern recognition receptor (PRR)-related mRNAs expression was up-regulated in AMI group compared with SA and control groups. Most toll-like receptor (TLR) mRNAs expression was significantly up-regulated (P<0.01) than the SA and control groups;macrophage scavenger receptor (MSR) mRNA was significantly up-regulated in AMI group compared with the control group (P<0.01), and the SA group showed an upward trend compared with the controls. Conclusions The expression of most neutrophil and mononuclear-macrophage function related genes mRNAs was significantly up-regulated by stages during the progression of CAD, suggesting that the adhesive, chemotactic and phagocytic functions of neutrophil and mononuclear-ma-crophage were strengthened in the occurrence and development of coronary atherosclerosis and AMI. This also showed a stepped up-ward trend as the disease progressed.