Abstract
The Effect of Interleukin-6-Type Cytokines and Adiponectin on MAPK Activation in the Immortalized Human Chondrocyte C28/I2 Line and Normal Human Chondrocytes
Highlights
Rheumatoid arthritis (RA) is a debilitating chronic inflammatory disease of synovial joints which over time alters the structure of articular cartilage and subchondral bone resulting in joint destruction
The principal objective of this study was to determine if recombinant human IL-6 and another cytokine related to IL6, namely, rhOSM as well as the adipokine, rhAPN, the latter which interact with receptors distinctly different from the IL-6/ IL-6R/gp130 complex, membrane IL-6R or soluble IL-6R, phosphorylate ERK1/2, JNK1/2 and p38α MAPK [21] in human chondrocyte cultures
The overarching hypothesis that was tested in this study was that treatment of C28/I2 chondrocytes with recombinant human IL-6 (rhIL-6), rhOSM or rhAPN would result in the phosphorylation of ERK1/2, JNK1/2 and p38α MAPK, without altering the level of total unphosphorylated ERK1/2, JNK1/2, and p38α MAPK
Summary
Rheumatoid arthritis (RA) is a debilitating chronic inflammatory disease of synovial joints which over time alters the structure of articular cartilage and subchondral bone resulting in joint destruction. Over the past 15 years or so different clinical approaches to the treatment of RA with a pro-inflammatory cytokine receptor antagonist fusion protein, small molecule inhibitors, and anti-cytokine receptor monoclonal antibodies have been employed. These drugs were developed by identifying molecular targets which are key mediators in the pathogenesis and progression of RA [1,2,3,4]. There is much more to be learned about the signal transduction pathways involved in the initiation and progression of RA, especially how dysfunctional signal transduction alters articular chondrocyte homeostasis [5,6]. A further analysis of signal transduction may reveal potential novel molecular targets for pharmacological intervention in RA necessary for inducing apoptosis of activated T- and B-cells, dendritic cells, neutrophils, macrophages and synoviocytes, while minimizing or inhibiting chondrocyte and osteocyte apoptosis [6,7,8,9]
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