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Differential up-regulation of the three TGF-β isoforms in human osteoarthritic cartilage
  1. Manuel Pombo-Suarez (maposu{at}
  1. Hospital Clinico Universitario de Santiago, Spain
    1. Maria Teresa Castaño-Oreja (cmmaite{at}
    1. University of Santiago de Compostela, Spain
      1. Manuel Calaza (mcalaza{at}
      1. Hospital Clinico Universitario de Santiago, Spain
        1. Juan J Gomez-Reino (juan.jesus.gomez-reino.carnota{at}
        1. Hospital Clinico Universitario de Santiago, Spain
          1. Antonio Gonzalez (antonio.gonzalez.martinez-pedrayo{at}
          1. Hospital Clinico Universitario de Santiago, Spain


            Objectives: Decreased levels of TGF-β have been related with failure of cartilage repair in experimental models of osteoarthritis (OA). We aimed to examine this aspect of OA in human cartilage.

            Methods: Cartilage samples were obtained from 11 patients with hip OA and 11 patients with femoral neck fracture that were undergoing total hip replacement. Gene expression of the 3 TGF-β isoforms, collagen type II (COL2A1) and aggrecan (AGC1) was analyzed by RT-qPCR and immunohistochemistry.

            Results: Expression of the three TGF-β isoforms was increased in OA cartilage. The up-regulation was more marked for the TGF-β3 isoform (2.3 fold) than for TGF-β1 (1.6 fold) or TGF-β2 (1.7 fold). The mRNA levels of TGF-β1 and TGF-β2 were strongly correlated in OA cartilage (rs = 0.83, p = 0.002), but levels of TGF-β3 were uncorrelated to any of the two other TGF-β isoforms. Immunohistochemistry showed an extension of immunoreactivity for the three TGF-β isoforms to more chondrocytes and to deeper cartilage layers in the more severe OA lesions. No correlation of TGF-£] isoforms with COL2A1 or AGC1 expression levels was found.

            Conclusions: The three isoforms of TGF-β were differentially up-regulated in late OA in relation with an increased percentage of TGF-β positive chondrocytes. These results indicate that cartilage damage progress in spite of the TGF-β stimulus for cartilage anabolism and that other causes of the failure to cope with the increased cartilage catabolism of OA should be investigated.

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