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. Author manuscript; available in PMC: 2011 Jul 1.
Published in final edited form as: Arthritis Rheum. 2010 Jul;62(7):2004–2012. doi: 10.1002/art.27475

Figure 3.

Figure 3

TLR2/TLR4- and MyD88-dependent pro-catabolic responses to endogenous degraded HA. Immature mouse chondrocytes isolated from MyD88−/−, TLR2/TLR4−/− and congenic WT mice were transfected with hyal2 cDNA, with an empty vector plasmid DNA used as a control. Forty-eight hours after transfection, the cells were placed onto poly-HEME coated plates. After three more days, degradation of HA (A) was confirmed from the conditioned media of chondrocytes by ELISA analysis. The conditioned media were analyzed for release of NO (B), MMP-3 and MMP-13 (C). Data for degradation of HA (n=3), for NO release from chondrocytes (n=3), and for MMP-3 and MMP-13 release from chondrocytes were representative of 3 individual experiments. Statistics for concentration of degraded HA in A, * p<0.04 relative to the vector control. Statistics for NO release in B, #, ## p<0.02 for hyal2 transfected MyD88−/− and TLR2/TLR4−/− relative to WT chondrocytes, respectively.