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Background: The metabolism of cholesteryl esters (CEs) is under the control of a gene network in macrophages. Several genes such as ATF3 and EGR2 are related to cholesterol metabolism. Methods: In this study, the ATF3 and EGR2 gene expression levels were evaluated in differentiated macrophages of subjects undergoing coronary artery angiography [controls (<5% stenosis), patients (>70% stenosis)] after treatment with small dense low density lipoprotein (sdLDL) particles. Monocytes were isolated using a RosetteSep Kit and were differentiated into macrophages using the M-CSF factor. A modified heparin-MgSO4-PEG method was used for the sdLDL preparation. The ATF3 and EGR2 gene expression levels were measured by the real-time quantitative polymerase chain reaction (RT-qPCR) technique. Results: In contrast with the control group (p=0.4), the ATF3 expression level reduced significantly in the differentiated macrophages from all patients [single vessel disease (SVD), fold change 17 times, p=0.02; two vessel disease (2VD), fold change 1.5 times, p=0.05; three vessel disease (3VD), fold change 3.5 times, p=0.04]. Also, the EGR2 expression level reduced significantly in all groups (p<0.02). The gene fold changes had no significant differences between the patients (p>0.8). Conclusions: We propose that the failure of ATF3 gene expression improves the CE synthesis after sdLDL influx. Furthermore, the reduced EGR2 gene expression level in the sdLDL-treated groups may be a negative factor in cholesterol homeostasis.

ATF3 and EGR2 gene expression levels in sdLDL-treated macrophages of patients with coronary artery stenosis