PMID- 27604056
OWN - NLM
STAT- MEDLINE
DCOM- 20170328
LR  - 20170817
IS  - 1473-5830 (Electronic)
IS  - 0954-6928 (Linking)
VI  - 28
IP  - 1
DP  - 2017 Jan
TI  - Altered human neutrophil FcgammaRI and FcgammaRIII but not FcgammaRII expression is 
      associated with the acute coronary event in patients with coronary artery 
      disease.
PG  - 63-69
AB  - OBJECTIVE: Neutrophils enhancing atherosclerotic plaque instability have been 
      observed in patients with acute coronary syndrome (ACS). Generally, activation of 
      neutrophils in lesions depends on the interaction of Fcgamma receptors (FcgammaRs) with 
      immunoglobulin G antibodies in immune complexes. However, altered FcgammaR expression 
      on neutrophils of patients with ACS is unknown. We aimed to evaluate changes in 
      FcgammaR expression on neutrophils of patients with ACS. METHODS: We enrolled 106 
      patients who were divided into four groups: acute myocardial infarction (AMI), 
      unstable angina (UA), stable angina, and normal coronary arteries. The 
      expressions of FcgammaRI, FcgammaRII, and FcgammaRIII on neutrophils and related upstream 
      ligand and downstream molecules were measured by flow cytometry and enzyme-linked 
      immunosorbent assay. RESULTS: The expression of unbound FcgammaRI was significantly 
      decreased in AMI and UA patients and that of unbound FcgammaRIII was significantly 
      decreased in AMI patients, with no difference in the expression of unbound FcgammaRII 
      among the four groups. In contrast, plasma levels of antioxidized LDL antibody, 
      myeloperoxidase, matrix metalloproteinase-9, and neutrophil gelatinase-associated 
      lipocalin were significantly greater in AMI and UA than in stable angina and 
      normal coronary arteries patients. CONCLUSION: Unbound FcgammaRI and FcgammaRIII 
      expression was decreased on neutrophils of patients with ACS, which reflects a 
      potential role of disturbed FcgammaRI and FcgammaRIII expression in the destabilization 
      of atherosclerotic plaque. Our findings may provide insight into the mechanism 
      underlying culprit plaque-relevant activation of neutrophil FcgammaRs in ACS 
      patients.
FAU - Zhao, Na
AU  - Zhao N
AD  - aDepartment of Cardiovascular Medicine, Shaanxi Province People's Hospital 
      Departments of bCardiovascular Medicine cHepatobiliary Surgery ICU, First 
      Affiliated Hospital of Medical College, Xi'an Jiaotong University dDepartment of 
      Ophthalmology Medicine, Xi'an IV People's Hospital, Xi'an, Shaanxi eKey 
      Laboratory of Carcinogenesis and Translational Research (Ministry of Education), 
      Department of Medical Affairs, Peking University Cancer Hospital & Institute, 
      Beijing, China.
FAU - Mi, Lan
AU  - Mi L
FAU - Zhang, Yaping
AU  - Zhang Y
FAU - Li, Na
AU  - Li N
FAU - Xu, Jiaojiao
AU  - Xu J
FAU - Xia, Dongyu
AU  - Xia D
FAU - Wang, Junkui
AU  - Wang J
FAU - Wu, Yue
AU  - Wu Y
FAU - Liu, Xiaojun
AU  - Liu X
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - England
TA  - Coron Artery Dis
JT  - Coronary artery disease
JID - 9011445
RN  - 0 (Biomarkers)
RN  - 0 (FCGR1A protein, human)
RN  - 0 (Receptors, IgG)
SB  - IM
MH  - Acute Coronary Syndrome/*blood/diagnosis
MH  - Aged
MH  - Angina, Stable/*blood/diagnosis
MH  - Angina, Unstable/*blood/diagnosis
MH  - Biomarkers/blood
MH  - Coronary Angiography
MH  - Coronary Artery Disease/*blood/diagnosis
MH  - Down-Regulation
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Flow Cytometry
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/*blood/diagnosis
MH  - Neutrophil Activation
MH  - Neutrophils/*metabolism
MH  - Prognosis
MH  - Receptors, IgG/*blood
EDAT- 2016/09/08 06:00
MHDA- 2017/03/30 06:00
CRDT- 2016/09/08 06:00
PHST- 2016/09/08 06:00 [pubmed]
PHST- 2017/03/30 06:00 [medline]
PHST- 2016/09/08 06:00 [entrez]
AID - 10.1097/MCA.0000000000000425 [doi]
PST - ppublish
SO  - Coron Artery Dis. 2017 Jan;28(1):63-69. doi: 10.1097/MCA.0000000000000425.