Free Thiol β2-GPI (β-2-Glycoprotein-I) Provides a Link Between Inflammation and Oxidative Stress in Atherosclerotic Coronary Artery Disease.


Journal

Arteriosclerosis, thrombosis, and vascular biology
ISSN: 1524-4636
Titre abrégé: Arterioscler Thromb Vasc Biol
Pays: United States
ID NLM: 9505803

Informations de publication

Date de publication:
11 2020
Historique:
pubmed: 18 9 2020
medline: 15 12 2020
entrez: 17 9 2020
Statut: ppublish

Résumé

Atherosclerotic coronary artery disease is well recognised as an inflammatory disorder that is also influenced by oxidative stress. β2-GPI (β-2-glycoprotein-I) is a circulating plasma protein that undergoes post-translational modification and exists in free thiol as well as oxidized forms. The aim of this study was to assess the association between these 2 post-translational redox forms of β2-GPI and atherosclerotic coronary artery disease. Approach and Results: Stable patients presenting for elective coronary angiography or CT coronary angiography were prospectively recruited. A separate group of patients after reperfused ST-segment-elevation myocardial infarction formed an acute coronary syndrome subgroup. All patients had collection of fasting serum and plasma for quantification of total and free thiol β2-GPI. Coronary artery disease extent was quantified by the Syntax and Gensini scores. A total of 552 patients with stable disease and 44 with acute coronary syndrome were recruited. While total β2-GPI was not associated with stable coronary artery disease, a higher free thiol β2-GPI was associated with its presence and extent. This finding remained significant after correcting for confounding variables, and free thiol β2-GPI was a better predictor of stable coronary artery disease than hs-CRP (high-sensitivity C-reactive protein). Paradoxically, there were lower levels of free thiol β2-GPI after ST-segment-elevation myocardial infarction. Free thiol β2-GPI is a predictor of coronary artery disease presence and extent in stable patients. Free thiol β2-GPI was a better predictor than high-sensitivity C-reactive protein.

Identifiants

pubmed: 32938215
doi: 10.1161/ATVBAHA.120.315156
doi:

Substances chimiques

Biomarkers 0
Inflammation Mediators 0
Lipids 0
beta 2-Glycoprotein I 0
C-Reactive Protein 9007-41-4

Types de publication

Comparative Study Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2794-2804

Auteurs

James C Weaver (JC)

University of NSW, Sydney, Australia (J.C.W., I.U., M.Q., B.G., K.A.R., S.A.K.).
Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, Sydney, Australia (J.C.W.).

Inaam Ullah (I)

University of NSW, Sydney, Australia (J.C.W., I.U., M.Q., B.G., K.A.R., S.A.K.).
Department of Cardiology, St George Hospital, Kogarah, Sydney, Australia (I.U.).

Miao Qi (M)

University of NSW, Sydney, Australia (J.C.W., I.U., M.Q., B.G., K.A.R., S.A.K.).
Department of Infectious Disease, Immunology and Sexual Health, St George Hospital, Kogarah, Sydney, Australia (M.Q., B.G., S.A.K.).

Bill Giannakopoulos (B)

University of NSW, Sydney, Australia (J.C.W., I.U., M.Q., B.G., K.A.R., S.A.K.).
Department of Infectious Disease, Immunology and Sexual Health, St George Hospital, Kogarah, Sydney, Australia (M.Q., B.G., S.A.K.).
Department of Rheumatology, St George Hospital, Kogarah, Sydney, Australia (B.G.).

Kerry Anne Rye (KA)

University of NSW, Sydney, Australia (J.C.W., I.U., M.Q., B.G., K.A.R., S.A.K.).

Maaike Kockx (M)

ANZAC Research Institute, University of Sydney, Concord, Australia (M.K., L.K.).

Leonard Kritharides (L)

ANZAC Research Institute, University of Sydney, Concord, Australia (M.K., L.K.).
Department of Cardiology, Concord Hospital, Sydney, Australia (L.K.).

Steven A Krilis (SA)

University of NSW, Sydney, Australia (J.C.W., I.U., M.Q., B.G., K.A.R., S.A.K.).
Department of Infectious Disease, Immunology and Sexual Health, St George Hospital, Kogarah, Sydney, Australia (M.Q., B.G., S.A.K.).

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Classifications MeSH