Interleukin-10 does not affect IL-1-induced interleukin-6 and metalloproteinase production in human chondrosarcoma cells, SW1353.

@article{Radons2006Interleukin10DN,
  title={Interleukin-10 does not affect IL-1-induced interleukin-6 and metalloproteinase production in human chondrosarcoma cells, SW1353.},
  author={Jürgen Radons and Werner Falk and Thomas E O Schubert},
  journal={International journal of molecular medicine},
  year={2006},
  volume={17 2},
  pages={
          377-83
        }
}
Cartilage repair by transplantation of autologous chondrocytes is an option when restoring functional joints. Control of chondrocyte function is thus required. Interleukin-10 (IL-10) is a potent anti-inflammatory cytokine affecting the expression of a wide range of immune mediators in hematopoietic and non-hematopoietic cells. Previous studies indicated that IL-10 has therapeutic potential in the treatment of chronic inflammatory joint disorders such as rheumatoid arthritis and osteoarthritis… Expand
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Inflammatory stress and sarcomagenesis: a vicious interplay
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References

SHOWING 1-10 OF 41 REFERENCES
IL-6 production by human articular chondrocytes. Modulation of its synthesis by cytokines, growth factors, and hormones in vitro.
TLDR
Chondrocytes probably contribute to the increased synovial fluid levels of IL-6 in inflammatory and degenerative conditions of cartilage, and IL- 6 may serve as a mediator to coordinate responses to cartilage injury. Expand
Role of interleukin-4 and interleukin-10 in murine collagen-induced arthritis. Protective effect of interleukin-4 and interleukin-10 treatment on cartilage destruction.
TLDR
The data are consistent with a dominant role of IL-10 in the natural suppression of arthritis expression, whereas combined treatment with IL-4 andIL-10 appears of potential therapeutic value, not only at the onset, but also in established arthritis. Expand
Mithramycin downregulates proinflammatory cytokine-induced matrix metalloproteinase gene expression in articular chondrocytes
TLDR
Despite effective inhibition of MMP expression by mithramycin and its potential to reduce cartilage degeneration, the agent might work through multiple unidentified mechanisms. Expand
The differential effects of IL-1 and TNF-α on proinflammatory cytokine and matrix metalloproteinase expression in human chondrosarcoma cells
TLDR
IL-1 and TNF-α each activate a distinct set of genes in chondrosarcoma cells, and gene expression in these cells is regulated by groups of genes related in part by their function. Expand
Effect of IL-1alpha on the expression of cartilage matrix proteins in human chondrosarcoma cell line OUMS-27.
TLDR
The results suggest that IL-1alpha suppresses the expression of cartilage matrix proteins through a suppression of the autocrine action of BMP-2, brought about by the decrease in B MP-2 receptor expression in chondrocytes. Expand
Early response genes induced in chondrocytes stimulated with the inflammatory cytokine interleukin-1beta
TLDR
This analysis identified alterations in the expression of multiple transcription factors, cytokines, growth factors and their receptors, adhesion molecules, proteases, and signaling intermediates that may contribute to inflammation and cartilage destruction in arthritis. Expand
Interleukin-10 and the interleukin-10 receptor.
TLDR
Findings that have advanced the understanding of IL-10 and its receptor are highlighted, as well as its in vivo function in health and disease. Expand
Interleukin-10 Therapy—Review of a New Approach
TLDR
New insight is given into the immunobiology of IL-10 and it is suggested that the IL- 10/IL-10 receptor system may become a new therapeutic target. Expand
Inhibition of cartilage destruction by double gene transfer of IL-1Ra and IL-10 involves the activin pathway
TLDR
Results demonstrate not only that virus-based gene transfer using a combination of two joint-protective genes is a feasible approach to inhibit cartilage degradation by activated RA synovial fibroblasts, but also that the underlying molecular effects include modulation of the activin pathway. Expand
Direct protective effect of interleukin-10 on articular chondrocytes in vitro.
TLDR
IL-10 not only inhibits the synthesis of inflammatory cytokines, but also directly protects chondrocytes by antagonizing IL-1 and inhibiting NOS2 and MMP3 expression. Expand
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4
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