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The involvement of CD36 in monocyte activation by antiphospholipid antibodies

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Title: The involvement of CD36 in monocyte activation by antiphospholipid antibodies
Authors: Kato, M. Browse this author
Atsumi, T. Browse this author →KAKEN DB
Oku, K. Browse this author
Amengual, O. Browse this author
Nakagawa, H. Browse this author
Fujieda, Y. Browse this author
Otomo, K. Browse this author
Horita, T. Browse this author
Yasuda, S. Browse this author
Koike, T. Browse this author →KAKEN DB
Keywords: Antiphospholipid syndrome
lupus anticoagulant
scavenger receptor
Issue Date: Jul-2013
Publisher: Sage publications ltd
Journal Title: Lupus
Volume: 22
Issue: 8
Start Page: 761
End Page: 771
Publisher DOI: 10.1177/0961203313490242
PMID: 23817509
Abstract: Background CD36, known as a scavenger receptor, is a transmembrane glycoprotein expressed on monocytes, platelets and endothelial cells, recognizes multiple ligands, including phosphatidylserine, and regulates atherogenesis and thrombosis. The objective of this study is to investigate the possible involvement of CD36 in the pathophysiology of thrombosis in patients with antiphospholipid syndrome (APS). Methods First, rs3765187, a missense mutation linked to CD36 deficiency, was investigated by TaqMan polymerase chain reaction (PCR) genotyping method in 819 Japanese, including 132 patients with APS, 265 with systemic lupus erythematosus (SLE) in the absence of APS, and 422 healthy subjects. Then, the involvement of CD36 in antiphospholipid antibody (aPL)-induced tissue factor (TF) expression was examined using CD36-null mice or anti-CD36. Purified IgG from patients with APS and a monoclonal phosphatidylserine-dependent antiprothrombin antibody were used in these experiments. TF expression was tested by real-time PCR and flow cytometry. Results Minor allele carrier of rs3765187 was less frequent in patients with APS (3.8% p=0.032), but not in patients with SLE in the absence of APS (7.9% p=0.32), compared with healthy subjects (10.2%). The aPL-induced TF expression was significantly suppressed on peritoneal macrophages from CD36-null mice compared to wild type and significantly inhibited by anti-CD36 on human monocytes. Conclusions The gene mutation linked to CD36 deficiency was less frequent in patients with APS. The deficient or suppressed CD36 function significantly reduced aPL-induced TF expression invitro. Taken together, in a susceptible background CD36 scavenger receptor function may be involved in the thrombotic pathophysiology in patients with APS.
Rights: The final, definitive version of this paper has been published in Lupus, 22(8), Jul. 2013 by SAGE Publications Ltd, All rights reserved. © 2013 SAGE Publications
Type: article (author version)
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 加藤 将

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