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van de Loo, F.A. et al.

Fons A. J. van de Loo, Sharon Veenbergen, Ben van den Brand, Miranda B. Bennink, Esmeralda Blaney-Davidson, Onno J. Arntz, Henk M. van Beuningen, Peter M. van der Kraan, Wim B. van den Berg, Sharon Veenbergen, Ben van den Brand, Miranda B. Bennink, Esmeralda Blaney-Davidson, Onno J. Arntz, Henk M. van Beuningen, Peter M. van der Kraan, Wim B. van den Berg,

Enhanced suppressor of cytokine signaling 3 in arthritic cartilage dysregulates human chondrocyte function.

OBJECTIVE: To determine the expression of suppressor of cytokine signaling 3 (SOCS-3) in human articular chondrocytes and its functional consequences. METHODS: Chondrocytes were isolated from the cartilage of patients with osteoarthritis (OA), patients with rheumatoid arthritis (RA), and trauma patients and from the healthy cartilage of patients with a femoral neck fracture. The human chondrocyte cell line G6 and primary bovine chondrocytes were used in validation experiments. SOCS-3 messenger RNA (mRNA) expression was measured by quantitative polymerase chain reaction, and SOCS-3 protein levels were determined by Western blotting and immunohistochemical analysis. To ascertain the role of SOCS-3 in the chondrocyte response to interleukin-1β (IL-1β) or lipopolysaccharide (LPS), the expression of SOCS3 was either reduced by small interfering RNA or enhanced by viral transduction. RESULTS: The expression of SOCS-3 mRNA (but not that of SOCS-1 mRNA) was significantly enhanced in chondrocytes obtained from OA cartilage (mean ± SD ΔC(t) 3.4 ± 1.0) and RA cartilage (ΔC(t) 3.4 ± 1.4) compared with cartilage obtained from patients with femoral neck fracture (ΔC(t) 5.3 ± 1.2). The expression of SOCS3 correlated significantly with that of other genes known to be expressed in arthritic chondrocytes, such as MMP13 (r = 0.743), ADAMTS4 (r = 0.779), and ADAMTS5 (r = 0.647), and an inverse relationship was observed with COL2A1 (r = -0.561). Up-regulation of SOCS-3 by IL-1 in G6 chondrocytes and its spontaneous expression in OA chondrocytes were reduced by mithramycin, a specific inhibitor of transcription factor Sp-1. Overexpression of SOCS-3 in bovine chondrocytes reduced IL-1- and LPS-induced nitric oxide production and insulin-like growth factor 1-induced proteoglycan synthesis. Interestingly, a similar impairment of function was observed in OA chondrocytes, which was partially restored by SOCS-3 gene knockdown. CONCLUSION: This study demonstrated that both SOCS-3 mRNA and SOCS-3 protein are expressed in human arthritic chondrocytes and affect cellular responses involved in cartilage pathology.[1]

References

Enhanced suppressor of cytokine signaling 3 in arthritic cartilage dysregulates human chondrocyte function. van de Loo, F.A., Veenbergen, S., van den Brand, B., Bennink, M.B., Blaney-Davidson, E., Arntz, O.J., van Beuningen, H.M., van der Kraan, P.M., van den Berg, W.B. Arthritis Rheum. (2012) [Pubmed]

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