p38/NF-kB-dependent expression of COX-2 during differentiation and inflammatory response of chondrocytes. (Articolo in rivista)

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  • p38/NF-kB-dependent expression of COX-2 during differentiation and inflammatory response of chondrocytes. (Articolo in rivista) (literal)
Anno
  • 2008-01-01T00:00:00+01:00 (literal)
Alternative label
  • Ulivi V. 1,2, Giannoni P. 3, Gentili C. 1, Cancedda R. 1,2, Descalzi F. 1,4 (2008)
    p38/NF-kB-dependent expression of COX-2 during differentiation and inflammatory response of chondrocytes.
    in Journal of cellular biochemistry (Print)
    (literal)
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  • Ulivi V. 1,2, Giannoni P. 3, Gentili C. 1, Cancedda R. 1,2, Descalzi F. 1,4 (literal)
Pagina inizio
  • 1393 (literal)
Pagina fine
  • 1406 (literal)
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  • 104 (literal)
Rivista
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  • Corresponding author: F. Descalzi Cancedda (fiorella.descalzi@istge.it). I.F.: 3.540 (literal)
Note
  • ISI Web of Science (WOS) (literal)
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  • 1. Istituto Nazionale per la Ricerca sul Cancro, Genova 2. Dipartimento di Oncologia, Biologia e Genetica, Università di Genova, Genova, 3. Biorigen Srl, Genova 4. Istituto Bioimmagini e Fisiologia Molecolare, Consiglio Nazionale delle Ricerche, Sezione di Genova, Genova (literal)
Titolo
  • p38/NF-kB-dependent expression of COX-2 during differentiation and inflammatory response of chondrocytes. (literal)
Abstract
  • Studying cartilage differentiation, we observed the emergence of inflammation-related proteins suggesting that a common pathway was activated in cartilage differentiation and inflammation. In the present paper, we investigated the expression pathway of the inflammation-related enzyme Cyclooxygenase-2 (COX-2) during differentiation and inflammatory response of the chondrocytic cell line MC615. Cells were cultured either as (i) proliferating prechondrogenic cells expressing type I collagen or (ii) differentiated hyperconfluent cells expressing Sox9 and type II collagen. The p38 and the NF-kB pathways were investigated in standard conditions and after inflammatory agents treatment. NF-kB was constitutively activated in differentiated cells. The activation level of NF-kB in differentiated cells was comparable to the level in proliferating cells treated with the inflammatory agent LPS. In both cases, p65 was bound to the NF-kB consensus sequence of COX-2 promoter. p38, constitutively activated in differentiated cells, was activated in proliferating cells by treatment with LPS or IL-1alpha. In stimulated proliferating cells the two pathways are connected since addition of the p38-specific inhibitor SB203580 inhibited p38 activation, significantly reduced NF-kB activation and repressed COX-2 synthesis indicating that p38 is upstream NF-kB activation and COX-2 synthesis. In differentiated cells, the treatment with the inflammatory agent neither enhance NF-kB activation, nor synthesis of COX-2 while the addition of SB203580 neither repressed activation of p38, nor COX-2 synthesis, suggesting a constitutive activation of a p38/NF-kB/COX2 pathway. Our data indicate that in chondrocytes, COX-2 is expressed via p38 activation/NF-kB recruitment during both differentiation and inflammatory response. J. Cell. Biochem. 104: 1393-1406, 2008. (c) 2008 Wiley-Liss, Inc. (literal)
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