Enhanced expression of mRNA for Krüppel-like factor 5 in CD34+ cells of the bone marrow in rheumatoid arthritis

S Hirohata¹, Y Miura², T Tomita³, H Yoshikawa³

¹ Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Kanagawa, Japan
² Faculty of Health Sciences, Kobe University School of Medicine, Kobe, Japan
³ Department of Orthopedic Surgery, Osaka University Medical School, Osaka, Japan

Correspondence to:
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@yahoo.co.jp

Accepted 2 September 2008

The first 150 words of the full text of this article appear below.

Bone marrow (BM) CD34+ cells in rheumatoid arthritis (RA) have abnormal capacities to respond to tumour necrosis factor alpha (TNF) 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 (NFB1) (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 NFB1 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 for their abnormal differentiation into fibroblast-like cells.

CD34+ cells . . . [Full text of this article]

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