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Abstract
ObjectivesThis study examined alterations in the functions and proteome of high-density lipoprotein (HDL) subfractions (HDL2 and HDL3) isolated from patients with acute coronary syndrome (ACS) compared with control subjects.MethodsWe measured HDL subfraction cholesterol efflux capacity, inflammatory index (HII), paraoxonase-1 (PON1) activity, and lipid hydroperoxide (LOOH) levels in both male age-matched controls and the ACS group (n = 40/group). Additionally, proteomic analysis was used to monitor changes in the HDL subfraction proteome between controls and ACS subjects.ResultsBoth HDL2 and HDL3 from ACS patients had greater HII and LOOH levels compared with controls (P<0.001); PON1 activity and cholesterol efflux capacity in both HDL2 and HDL3 from the ACS group were significantly less than those of controls (P<0.001). Using proteomic analysis, we demonstrated that, compared with the control group, nine proteins were selectively enriched in HDL3 from subjects with ACS, and ras-related protein Rab-7b was decreased in HDL3. Additionally, in the ACS subjects, 12 proteins were decreased in HDL2 and 4 proteins were increased in HDL2.ConclusionsFunctional HDL subfractions shifted to dysfunctional HDL subfractions during ACS, and the functional impairment was linked to remodeled protein cargo in HDL subfractions from ACS patients.
Highlights
A strong inverse correlation between high-density lipoprotein cholesterol (HDL-C) level and coronary artery disease (CAD) has fostered intensive research seeking to target HDL metabolism for therapeutic gain [1,2]
Our study demonstrated that functional HDL subfractions shifted to dysfunctional HDL subfractions during acute coronary syndrome (ACS) and that the functional impairment was linked to remodeled protein cargo in HDL subfractions from ACS patients
Compared with the control group, the cholesterol efflux rates in HDL, HDL2, and HDL3 from the ACS group were decreased by 28.4%, 25.6%, and 25.5%, respectively (P,0.001, Table 2 and Figure 1A); and the PON1 activities in HDL, HDL2, and HDL3 were decreased by 24.3%, 29.5%, and 27.5% compared with the controls, respectively (P,0.001, Table 2 and Figure 1C)
Summary
A strong inverse correlation between high-density lipoprotein cholesterol (HDL-C) level and coronary artery disease (CAD) has fostered intensive research seeking to target HDL metabolism for therapeutic gain [1,2]. HDL is thought to protect against atherosclerosis by promoting reverse cholesterol transport (RCT), potentially through anti-oxidative and anti-inflammatory capacities [3,4]. It appears that the relationship between HDL levels and CAD risk is more complex and not just merely related to the plasma HDL-C levels. Recent studies have suggested that the ability of HDL to promote RCT from macrophages correlates with atherosclerosis independent of HDL-C [4]. The assessment of HDL functions has become a novel target to investigate the association between HDL and CAD risk
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