4.7 Article

Infliximab reduces CD147, MMP-3, and MMP-9 expression in peripheral blood monocytes in patients with active rheumatoid arthritis

期刊

EUROPEAN JOURNAL OF PHARMACOLOGY
卷 698, 期 1-3, 页码 429-434

出版社

ELSEVIER
DOI: 10.1016/j.ejphar.2012.10.030

关键词

CD147; Matrix metalloproteinase; Rheumatoid arthritis; Infliximab; Therapy

资金

  1. Science Project of Guangdong Province, PR China [2008B060600033, 2007B031511008]

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Recent studies have reported elevated expression levels in active rheumatoid arthritis patients of the cluster of differentiation (CD) 147 on CD14(+) peripheral blood monocytes and as a result, CD147 may be a target for the development of a novel rheumatoid arthritis therapy. This report describes the inhibitory effects of infliximab on CD147 and metalloproteinases (MMP)-3 and MMP-9 overexpression in peripheral blood monocytes obtained from patients with active rheumatoid arthritis. Thirty patients with active rheumatoid arthritis that were refractory to methotrexate therapy were randomized at a 4:1 ratio into groups A and B, respectively. Group A received three to four infusions of infliximab (3 mg/kg) and group B participants received four infusions of placebo. Both groups were also treated with a stable background dose of methotrexate. The CD147 expression levels on CD14(+) peripheral blood monocytes of rheumatoid arthritis patients was detected by flow cytometry. The expression of CD147, MMP-3, and, MMP-9 mRNA in peripheral blood mononuclear cells was assayed by real-time quantitative PCR, and the expression of MMP-3 and MMP-9 in serum was measured by a multiplexed microsphere-based flow assay. Results showed that the expression of CD147 and MMP-9 mRNA in group A decreased compared to group B. Expression of CD147 on CD14(+) monocytes was reduced (P < 0.05), and serum MMP-3 and -9 levels in group A were decreased by week 18. These data suggested that infliximab could inhibit CD147 expression on CD14(+) monocytes as well as reduce the levels of MMP-3 and MMP-9 in peripheral blood monocytes. (c) 2012 Elsevier B.V. All rights reserved.

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