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Enhanced expression of mRNA for Krüppel-like factor 5 in CD34+ cells of the bone marrow in rheumatoid arthritis
  1. S Hirohata1,
  2. Y Miura2,
  3. T Tomita3,
  4. H Yoshikawa3
  1. 1
    Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Kanagawa, Japan
  2. 2
    Faculty of Health Sciences, Kobe University School of Medicine, Kobe, Japan
  3. 3
    Department of Orthopedic Surgery, Osaka University Medical School, Osaka, Japan
  1. Dr S Hirohata, Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, 1-15-1 Kitasato, Sagamihara, Kanagawa 228–8555 Japan; shunsei_tenpoint{at}

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Bone marrow (BM) CD34+ cells in rheumatoid arthritis (RA) have abnormal capacities to respond to tumour necrosis factor alpha (TNFα) and to differentiate into fibroblast-like cells producing matrix metalloproteinase type 1, suggesting that BM CD34+ progenitor cells might generate type B synoviocytes.1 Of note, RA BM CD34+ cells show enhanced expression of nuclear factor kappa B1 (NFκB1) (p50), the silencing of which resulted in the prevention of fibroblast-like cell differentiation.2 Krüppel-like factor 5 (KLF-5), a zinc finger-containing transcription factor, activates many genes, including platelet-derived growth factor (PDGF) A/B, plasminogen activator inhibitor-1, inducible nitric oxide synthase and vascular endothelial growth factor receptors.3 4 KLF-5 has been shown to cooperate with NFκB1 to activate PDGF-A gene expression,4 5 which might be involved in synovial fibroblast-like cell proliferation.6 We explored KLF-5 messenger RNA expression in RA BM CD34+ cells to delineate the mechanism …

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  • Competing interests: None.

  • Funding: This work was supported by a grant-in-aid from the Health Science Research grant from the Ministry of Health and Welfare of Japan and a grant from Astellas Pharma Inc, Tokyo, Japan.

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