Abstract
BackgroundCoronary heart disease (CHD) is an important complication of atherosclerosis. Biomarkers, which associate with CHD development, are potential to predict CHD risk. To determine whether genes showing altered expression in hyperlipidaemia (H) and coronary heart disease (CHD) patients compared with controls could be CHD risk biomarkers.MethodsControl, H, and CHD groups represented atherosclerosis to CHD development. Gene profiling was investigated in peripheral blood mononuclear cells using DNA microarrays. Eight selected genes expressed only in H and CHD groups were validated by real-time quantitative reverse transcription PCR and plasma protein determination.Resultsα-defensin (DEFA1/DEFA3), pro-platelet basic protein (PPBP), and beta and alpha2 hemoglobin mRNA expression was significantly increased in H and CHD groups compared with controls, but only plasma PPBP and α-defensin proteins were correspondingly increased.ConclusionPPBP and DEFA1/DEFA3 could be potential CHD biomarkers in Thai hyperlipidaemia patients.
Highlights
Coronary heart disease (CHD) is an important complication of atherosclerosis
We suggest that significantly increased expression of both pro-platelet basic protein (PPBP) and DEFA1/ DEFA3 and their encoded proteins has the potential to be established as a synergistic predictive biomarker for coronary heart disease (CHD) risk in hyperlipidaemia patients
We found that the mRNA expression of PPBP, DEFA1/DEFA3, HBA2, and HBB was significantly increased in H and CHD groups of patients compared with controls, plasma protein validation only revealed significant increases in PPBP and αdefensin 1–3
Summary
Coronary heart disease (CHD) is an important complication of atherosclerosis. To determine whether genes showing altered expression in hyperlipidaemia (H) and coronary heart disease (CHD) patients compared with controls could be CHD risk biomarkers. Atherosclerosis is a complicated, progressive disease characterized by the accumulation of lipids and fibrous elements in large and medium-sized arteries. It is the major underlying cause of cardiovascular disease (CVD), which in turn is the leading cause of death in the developed world, and an important cause of morbidity worldwide. Abundant previous studies have linked dyslipidaemia to atherogenesis, and roles have been identified for inflammatory mechanisms coupled with dyslipidaemia in atheroma formation both in humans and animal models [1,2,3]. Several clinical evaluations are available for patients with CVD and CHD, including diagnostic tests of varied accuracy, reproducibility, ease of use, and potential for patient morbidity [5]
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