Bioinformatics indicate that miR-223 regulates many genes associated with cholesterol metabolism, and it could also control high-density lipoprotein-cholesterol (HDL-C) uptake. As reported in previous study, miR-223 was found to be upregulated from human subjects with familial hypercholesterolaemia, however, it remains to be determined using a larger group of coronary heart disease (CHD) patients. Moreover, whether it correlates with severity of atherogenesis, has never been elucidated before. We aim to further explore the association between circulating miR-223 content and severity of CHD. Sample was collected from 300 CHD patients and 100 subjects with angiographic exclusion of CHD. MiR-223 content was detected using quantitative real-time PCR. Gensini score was used to evaluate the severity of coronary stenotic lesions. Expression of miR-223 was identified on basis of the quartiles of the Gensini score, and association between the miRNA and CHD was analyzed. Diagnostic potential of miR-223 of CHD was performed by ROC analysis. CHD patients had higher miR-223 level (13.23, 9.29-17.59 vs. 4.05, 3.06-6.11, p < .001), and the miRNA content significantly elevated following increasing Gensini score (p < .001). Gensini score was significantly associated with miR-223 expression (r= .7289, p < .001). The optimal cut-off value of miR-223 was with a sensitivity of 86.0% and specificity of 91.3%. The AUC of miR-223 was 0.933 (95%CI, 0.905-0.961). These preliminary results suggest that the expression of miR-223 may be associated with atherogenesis. The level of circulating miR-223 in predicting the severity of coronary atherosclerosis may have a relatively certain value.
Keywords: Coronary artery disease; atherosclerosis; cholesterol metabolism; microRNA-223; molecular diagnostics.