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Interleukin-4 antagonizes oncostatin M and transforming growth factor beta-induced responses in articular chondrocytes
Journal of cellular biochemistry, 2008-02, Vol.103 (2), p.588-597
El Mabrouk, Mohammed
Qureshi, Hamid Yaqoob
Li, Wen Qing
Sylvester, Judith
Zafarullah, Muhammad
2008
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
El Mabrouk, Mohammed
Qureshi, Hamid Yaqoob
Li, Wen Qing
Sylvester, Judith
Zafarullah, Muhammad
Titel
Interleukin-4 antagonizes oncostatin M and transforming growth factor beta-induced responses in articular chondrocytes
Ist Teil von
Journal of cellular biochemistry, 2008-02, Vol.103 (2), p.588-597
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2008
Quelle
Wiley Online Library All Journals
Beschreibungen/Notizen
Oncostatin M (OSM) stimulates cartilage degradation in rheumatoid arthritis (RA) by inducing matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS; a disintegrin and metalloproteinase with thrombospondin motif). Transforming growth factor beta (TGF‐β1) induces cartilage repair in joints but in excessive amounts, promotes inflammation. OSM and TGF‐β1 also induce tissue inhibitor of metalloproteinase‐3 (TIMP‐3), an important natural inhibitor of MMPs, aggrecanases, and tumor necrosis factor alpha converting enzyme (TACE), the principal proteases involved in arthritic inflammation and cartilage degradation. We studied cartilage protective mechanisms of the antiinflammatory cytokine, interleukin‐4 (IL‐4). IL‐4 strongly (MMP‐13 and TIMP‐3) or minimally (ADAMTS‐4) suppressed OSM‐induced gene expression in chondrocytes. IL‐4 did not affect OSM‐stimulated phosphorylation of extracellular signal‐regulated kinases (ERKs), protein 38 (p38), c‐Jun N‐terminal kinase (JNK) and Stat1. Lack of additional suppression with their inhibitors suggested that MMP‐13, ADAMTS‐4, and TIMP‐3 inhibition was independent of these mediators. IL‐4 also downregulated TGF‐β1‐induced TIMP‐3 gene expression, Smad2, and JNK phosphorylation. Additional suppression of TIMP‐3 RNA by JNK inhibitor suggests JNK implication. The cartilage protective effects of IL‐4 in animal models of arthritis may be due to its inhibition of MMPs and ADAMTS‐4 expression. However, suppression of TIMP‐3 suggests caution for using IL‐4 as a cartilage protective therapy. J. Cell. Biochem. 103: 588–597, 2008. © 2007 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0730-2312
eISSN: 1097-4644
DOI: 10.1002/jcb.21434
Titel-ID: cdi_proquest_miscellaneous_70227984
Format
–
Schlagworte
ADAM Proteins - biosynthesis
,
ADAM Proteins - genetics
,
ADAMTS4 Protein
,
Animals
,
Cartilage, Articular - cytology
,
Cartilage, Articular - drug effects
,
Cattle
,
Cells, Cultured - drug effects
,
Chondrocytes - drug effects
,
Chondrocytes - metabolism
,
Down-Regulation
,
Gene Expression Regulation - drug effects
,
interleukin-4
,
Interleukin-4 - pharmacology
,
joint damage
,
Matrix Metalloproteinase 13 - biosynthesis
,
Matrix Metalloproteinase 13 - genetics
,
Mitogen-Activated Protein Kinases - biosynthesis
,
Mitogen-Activated Protein Kinases - genetics
,
oncostatin M
,
Oncostatin M - antagonists & inhibitors
,
Phosphorylation - drug effects
,
Procollagen N-Endopeptidase - biosynthesis
,
Procollagen N-Endopeptidase - genetics
,
proteases
,
Protein Kinase Inhibitors - pharmacology
,
Protein Processing, Post-Translational - drug effects
,
Recombinant Proteins - antagonists & inhibitors
,
rheumatoid arthritis
,
RNA, Messenger - biosynthesis
,
Signal Transduction - drug effects
,
Smad2 Protein - biosynthesis
,
Smad2 Protein - genetics
,
STAT1 Transcription Factor - antagonists & inhibitors
,
STAT1 Transcription Factor - biosynthesis
,
STAT1 Transcription Factor - genetics
,
Tissue Inhibitor of Metalloproteinase-3 - biosynthesis
,
Tissue Inhibitor of Metalloproteinase-3 - genetics
,
Transforming Growth Factor beta - antagonists & inhibitors
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