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. 2006 Dec 20;66(6):782–789. doi: 10.1136/ard.2006.060269

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Figure 4 Reversal of interferon γ (IFNγ)‐mediated matrix metalloproteinase 13 (MMP13) suppression by signal transducer and activator of transcription (STAT)‐1 knockdown. (A) Cells were either mock transfected (control) or transfected with negative control and STAT1‐specific small interfering RNA (siRNA), incubated for 48 h and lysates subjected to western blotting with STAT1 and p44/42 mitogen‐activated protein kinase (MAPK) antibodies. (B) Chondrocytes transfected with STAT1 or control siRNA were analysed for MMP13 and glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) gene expression by reverse transcriptase ‐PCR and MMP13 protein. (C) Chondrocytes were cotransfected with control or STAT1 siRNA, along with MMP13 promoter‐luciferase vector. Luciferase activity from cell lysates is depicted as bar graphs. (D) Chondrocytes were pretreated with fludarabine (15 μM) for 6 and 24 h, treated with IFNγ for 15 min and cell lysates used for STAT1 tyrosine (tyr)/serine (ser) phosphporylation or total STAT1 and p44/42 MAPK analysis. (E) Cells pretreated with fludarabine were incubated with IFNγ and ILβ for 24 h and MMP13 and GAPDH mRNA and MMP13 protein analysed.