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Gene Review

OSM  -  oncostatin M

Bos taurus

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Disease relevance of OSM


High impact information on OSM


Biological context of OSM


Anatomical context of OSM

  • We examined responsiveness of the TIMP-3 gene to OSM in articular chondrocytes and studied the regulatory and signaling mechanisms of this response [1].
  • In addition, OSM stimulated endothelial cell proliferation and migration as well as acquisition of a spindle shape [2].
  • METHODS: Bovine articular cartilage explants were cultured in the presence of interleukin 1a, oncostatin M, and plasminogen to induce cartilage degradation [5].

Associations of OSM with chemical compounds

  • OBJECTIVES: Retinoic acid (RetA) and oncostatin M (OSM) have both been shown to mediate potent effects with respect to extracellular matrix integrity [6].
  • METHODS: Animal and human cartilage samples were used to assess the ability of RetA + OSM to promote the release of collagen and proteoglycan fragments, which was determined by measuring glycosaminoglycan and hydroxyproline, respectively [6].

Regulatory relationships of OSM


Other interactions of OSM

  • The antibody bound to ovine and bovine submaxillary mucins (OSM and BSM) [7].
  • Suboptimal doses of IL17 synergised potently with TNFalpha, IL1, OSM, and IL6 to promote collagen degradation [8].
  • Transforming growth factor beta1 blocks the release of collagen fragments from boving nasal cartilage stimulated by oncostatin M in combination with IL-1alpha [9].

Analytical, diagnostic and therapeutic context of OSM

  • Western blot analysis demonstrated that OSM stimulated predominantly the synthesis of a 22 kDa form of bFGF [2].
  • OSM treatment of BAE cells enhanced the synthesis of bFGF protein as determined by ELISA assays [2].


  1. Oncostatin M up-regulates tissue inhibitor of metalloproteinases-3 gene expression in articular chondrocytes via de novo transcription, protein synthesis, and tyrosine kinase- and mitogen-activated protein kinase-dependent mechanisms. Li, W.Q., Zafarullah, M. J. Immunol. (1998) [Pubmed]
  2. Oncostatin M induces basic fibroblast growth factor expression in endothelial cells and promotes endothelial cell proliferation, migration and spindle morphology. Wijelath, E.S., Carlsen, B., Cole, T., Chen, J., Kothari, S., Hammond, W.P. J. Cell. Sci. (1997) [Pubmed]
  3. Effects of ovariectomy and estrogen therapy on type II collagen degradation and structural integrity of articular cartilage in rats: implications of the time of initiation. Oestergaard, S., Sondergaard, B.C., Hoegh-Andersen, P., Henriksen, K., Qvist, P., Christiansen, C., Tankó, L.B., Karsdal, M.A. Arthritis Rheum. (2006) [Pubmed]
  4. Inhibition of furin-like enzymes blocks interleukin-1alpha/oncostatin M-stimulated cartilage degradation. Milner, J.M., Rowan, A.D., Elliott, S.F., Cawston, T.E. Arthritis Rheum. (2003) [Pubmed]
  5. Cartilage destruction in collagen induced arthritis assessed with a new biochemical marker for collagen type II C-telopeptide fragments. Ishikawa, T., Nishigaki, F., Christgau, S., Noto, T., Mo, J., From, N., Minoura, K., Hirayama, Y., Ohkubo, Y., Mutoh, S. J. Rheumatol. (2004) [Pubmed]
  6. Retinoic acid and oncostatin M combine to promote cartilage degradation via matrix metalloproteinase-13 expression in bovine but not human chondrocytes. Shingleton, W.D., Jones, D., Xu, X., Cawston, T.E., Rowan, A.D. Rheumatology (Oxford, England) (2006) [Pubmed]
  7. Mucin-carbohydrate directed monoclonal antibody. Kurosaka, A., Fukui, S., Kitagawa, H., Nakada, H., Numata, Y., Funakoshi, I., Kawasaki, T., Yamashina, I. FEBS Lett. (1987) [Pubmed]
  8. Interleukin 17 induces cartilage collagen breakdown: novel synergistic effects in combination with proinflammatory cytokines. Koshy, P.J., Henderson, N., Logan, C., Life, P.F., Cawston, T.E., Rowan, A.D. Ann. Rheum. Dis. (2002) [Pubmed]
  9. Transforming growth factor beta1 blocks the release of collagen fragments from boving nasal cartilage stimulated by oncostatin M in combination with IL-1alpha. Hui, W., Rowan, A.D., Cawston, T. Cytokine (2000) [Pubmed]
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