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dc.contributor.authorAhmed, Salahuddinen_US
dc.contributor.authorPakozdi, Angelaen_US
dc.contributor.authorKoch, Alisa E.en_US
dc.date.accessioned2007-09-18T19:23:34Z
dc.date.available2007-09-18T19:23:34Z
dc.date.issued2006-08en_US
dc.identifier.citationAhmed, Salahuddin; Pakozdi, Angela; Koch, Alisa E. (2006). "Regulation of interleukin-1Β–induced chemokine production and matrix metalloproteinase 2 activation by epigallocatechin-3-gallate in rheumatoid arthritis synovial fibroblasts." Arthritis & Rheumatism 54(8): 2393-2401. <http://hdl.handle.net/2027.42/55807>en_US
dc.identifier.issn0004-3591en_US
dc.identifier.issn1529-0131en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/55807
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=16869002&dopt=citationen_US
dc.description.abstractObjective To evaluate the efficacy of epigallocatechin-3-gallate (EGCG), a potent antiinflammatory molecule, in regulating interleukin-1Β (IL-1Β)–induced production of the chemokines RANTES (CCL5), monocyte chemoattractant protein 1 (MCP-1/CCL2), epithelial neutrophil–activating peptide 78 (ENA-78/CXCL5), growth-regulated oncogene Α (GROΑ/CXCL1), and matrix metalloproteinase 2 (MMP-2) activity in rheumatoid arthritis (RA) synovial fibroblasts. Methods Fibroblasts obtained from RA synovium were grown, and conditioned medium was obtained. Cell viability was determined by MTT assay. RANTES, MCP-1, ENA-78, and GROΑ produced in culture supernatants were measured by enzyme-linked immunosorbent assay. MMP-2 activity was analyzed by gelatin zymography. Western blotting was used to study the phosphorylation of protein kinase C (PKC) isoforms and nuclear translocation of NF-ΚB. Results EGCG was nontoxic to RA synovial fibroblasts. Treatment with EGCG at 10 Μ M or 20 Μ M significantly inhibited IL-1Β–induced ENA-78, RANTES, and GROΑ, but not MCP-1 production in a concentration-dependent manner. EGCG at 50 Μ M caused a complete block of IL-1Β–induced production of RANTES, ENA-78, and GROΑ, and reduced production of MCP-1 by 48% ( P < 0.05). Zymography showed that EGCG blocked constitutive, IL-1Β–induced, and chemokine-mediated MMP-2 activity. Evaluation of signaling events revealed that EGCG preferentially blocked the phosphorylation of PKCΔ and inhibited the activation and nuclear translocation of NF-ΚB in IL-1Β–treated RA synovial fibroblasts. Conclusion These results suggest that EGCG may be of potential therapeutic value in inhibiting joint destruction in RA.en_US
dc.format.extent638762 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
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dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.titleRegulation of interleukin-1Β–induced chemokine production and matrix metalloproteinase 2 activation by epigallocatechin-3-gallate in rheumatoid arthritis synovial fibroblastsen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelGeriatricsen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumUniversity of Michigan Medical School, Ann Arbor ; Department of Internal Medicine/Division of Rheumatology, University of Michigan Medical School, BSRB Room 4388, 109 Zina Pitcher Drive, Ann Arbor, MI 48109-2200en_US
dc.contributor.affiliationumUniversity of Michigan Medical School, Ann Arboren_US
dc.contributor.affiliationumVA Medical Center and University of Michigan Medical School, Ann Arbor, Michiganen_US
dc.identifier.pmid16869002en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/55807/1/22023_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/art.22023en_US
dc.identifier.sourceArthritis & Rheumatismen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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