title: Acute coronary syndrome remodels the protein cargo and functions of high-density lipoprotein subfractions.
abstract: OBJECTIVE
  This 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.
  
  
  METHODS
  We 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.
  
  
  RESULTS
  Both 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.
  
  
  CONCLUSIONS
  Functional 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.
authors.affiliation: Division of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Tan
authors.affiliation: Division of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China.
authors.forename: Ting Rong
authors.initials: TR
authors.lastname: Liu
authors.affiliation: Laboratory of Pathophysiology, Southern Medical University, Guangzhou, Guangdong, P.R. China.
authors.forename: Shui Wang
authors.initials: SW
authors.lastname: Hu
authors.affiliation: Division of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China.
authors.forename: Di
authors.initials: D
authors.lastname: Tian
authors.affiliation: Division of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China.
authors.forename: Chen
authors.initials: C
authors.lastname: Li
authors.affiliation: Division of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China.
authors.forename: Jian Kai
authors.initials: JK
authors.lastname: Zhong
authors.affiliation: Division of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China.
authors.forename: Hai Ge
authors.initials: HG
authors.lastname: Sun
authors.affiliation: Division of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China.
authors.forename: Tian Tian
authors.initials: TT
authors.lastname: Luo
authors.affiliation: Division of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China.
authors.forename: Wen Yan
authors.initials: WY
authors.lastname: Lai
authors.affiliation: Division of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China.
authors.forename: Zhi-Gang
authors.initials: ZG
authors.lastname: Guo
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood* / Q000378:metabolism*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D040901:Proteomics; D000683:Serum Amyloid P-Component / Q000378:metabolism; D020691:rab GTP-Binding Proteins / Q000097:blood; D000090802:rab7 GTP-Binding Proteins
chemical_list: D008075:Lipoproteins, HDL; D000683:Serum Amyloid P-Component; D000090802:rab7 GTP-Binding Proteins; D020691:rab GTP-Binding Proteins
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