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      1. Author :
        Evans, L.; Williams, A.S.; Hayes, A.J.; Jones, S.A.; Nowell, M.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Arthritis and Rheumatism
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Apo866; Arthritis; In vivo; Living Image software; MMPSense 750 FAST; Xenogen Caliper IVIS 200
      12. Abstract :
        OBJECTIVE: Using APO866, studies assessed the ability of Pre-B-cell colony-Enhancing Factor (PBEF) to regulate inflammatory and degradative processes in fibroblasts and collagen-induced arthritis. METHODS: ELISAs were used to examine regulation of metalloproteinases and chemokine expression by HFF fibroblasts. PBEF was further examined in the collagen-induced arthritis model using APO866. Disease activity was assessed using radiography, histology, in vivo imaging and quantitative PCR (qPCR). RESULTS: In vitro activation of fibroblasts with PBEF promoted MMP-3, CCL-2 and CXCL-8 expression, an effect inhibited by APO866. Early intervention with APO866 in collagen-induced arthritis inhibited both synovial inflammation, including chemokine-directed leukocyte infiltration, and the systemic marker of inflammation, serum hyaluronic acid. Blockade of degenerative processes by APO866 was further illustrated by the reduced expression of MMP-3 and MMP-13 in joint extracts and reduction of the systemic marker of cartilage erosion, serum cartilage oligomeric matrix protein (COMP). Radiology showed that APO866 protected against bone erosion, whilst qPCR demonstrated inhibition of RANKL expression. APO866 treatment in established disease (clinical score >=5) reduced synovial inflammation, cartilage destruction and halted bone erosion. MMP-3, CCL-2 and RANKL activity, as assessed by in vivo imaging with MMPSense750 and qPCR were reduced in treated animals. qPCR of synovial explants from animals with CIA showed that APO866 inhibited MMP-3, CCL-2 and RANKL production, a result that was reversed with nicotinamide mononucleotide (NMN) CONCLUSIONS: These data confirm PBEF to be an important regulator of inflammation, cartilage catabolism and bone erosion, and highlights APO866 as a promising therapy for targeting PBEF activity in inflammatory arthritis.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21400478
      14. Call Number :
        PKI @ user @ 8551
      15. Serial :
        4800
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