TAK1 mediates the collagen-II-dependent induction of the COX-2 gene and PGE2 release in primary human chondrocytes

We investigated the role of transforming growth factor-beta activated kinase 1 (TAK1) in collagen II signaling in primary human chondrocytes (PHCs). We asked whether TAK1 acts as a modulator of collagen II signaling with respect to collagen-II-dependent induction of cyclooxigenase-2 (COX-2) in PHCs...

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Bibliographic Details
Published in:Connective tissue research 2010-12, Vol.51 (6), p.452-458
Main Authors: Klatt, Andreas R., Klinger, Gabriele, Paul-Klausch, Brigitte, Renno, Joerg H., Schmidt, Joachim, Malchau, Gebhart, Wielckens, Klaus
Format: Article
Language:English
Subjects:
Cartilage, Articular - cytology
Cartilage, Articular - metabolism
Cartilage, Articular - pathology
Cells, Cultured
Chondrocytes - enzymology
Chondrocytes - secretion
collagen II
Collagen Type II - physiology
COX-2
Cyclooxygenase 2 - biosynthesis
Cyclooxygenase 2 - genetics
Dinoprostone - metabolism
Dinoprostone - secretion
Gene Expression Regulation - physiology
Gene Silencing - physiology
Humans
MAP Kinase Kinase Kinases - physiology
osteoarthritis
Osteoarthritis - genetics
Osteoarthritis - metabolism
Osteoarthritis - pathology
PHC
TAK1
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Summary:We investigated the role of transforming growth factor-beta activated kinase 1 (TAK1) in collagen II signaling in primary human chondrocytes (PHCs). We asked whether TAK1 acts as a modulator of collagen II signaling with respect to collagen-II-dependent induction of cyclooxigenase-2 (COX-2) in PHCs and release of PGE2 from PHCs. Therefore, PHCs were incubated with collagen II, and cells were then analyzed by RT-PCR for the expression of COX-2. ELISA was used to quantify PGE2 release. To examine the influence of TAK1 on these events, TAK1 gene silencing was performed by RNAi in PHCs prior to collagen II treatment. Results indicated that COX-2 gene expression and PGE2 release are specific outcomes of collagen II signaling and that both depend on TAK1 mediation. These findings are promising in that therapeutic inhibition of TAK1 might be used to reduce pain and relieve inflammatory symptoms that are common in osteoarthritis.
ISSN:0300-8207
1607-8438
DOI:10.3109/03008201003668360