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Rheumatology (Oxford). 2014 Dec;53(12):2288-96. doi: 10.1093/rheumatology/keu260. Epub 2014 Jul 21.

CD147 up-regulates calcium-induced chemotaxis, adhesion ability and invasiveness of human neutrophils via a TRPM-7-mediated mechanism.

Author information

1
Department of Clinical Immunology, Xijing Hospital and Department of Cell Biology/Cell Engineering Research Centre, Fourth Military Medical University, Xi'an, China.
2
Department of Clinical Immunology, Xijing Hospital and Department of Cell Biology/Cell Engineering Research Centre, Fourth Military Medical University, Xi'an, China. zhuping@fmmu.edu.cn.

Abstract

OBJECTIVES:

We aimed to investigate whether CD147 can up-regulate the chemotactic, adhesive and invasive properties of human neutrophils and to determine the mechanism underlying this process.

METHODS:

Human promyelocytic leukaemia cells (HL-60) cells and peripheral blood or synovial fluid neutrophils were isolated from RA patients. Under cyclophilin A (CypA) stimulation, chemotaxis, adhesion potential and invasion ability were assessed using chemotaxis, adhesion and invasiveness assays. Lipid raft isolation and western blot were used to determine the mechanism underlying the effects of CypA stimulation.

RESULTS:

CD147 up-regulates the calcium-induced chemotaxis, adhesion ability and invasiveness of human neutrophils in RA patients. Transient receptor potential melastatin 7 may be responsible for this phenomenon.

CONCLUSION:

These findings suggest that in RA patients, abundant CypA up-regulates the calcium-induced chemotactic, adhesive and invasive properties of neutrophils via direct binding to CD147. Cyclophilin-CD147 interactions might contribute to the destruction of cartilage and bone in RA.

KEYWORDS:

CD147; TRPM-7; calcium influx; neutrophil; rheumatoid arthritis

PMID:
25053832
DOI:
10.1093/rheumatology/keu260
[Indexed for MEDLINE]
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