Abstract
MMP-13 mRNA levels were increased by downregulation of p21, and this was reversed by treatment with a STAT3 inhibitor (Figure 2a, b). Downregulation of p21 also decreased proteoglycan synthesis (Figure 2c). In a mouse OA model and in human primary chondrocytes, we found that p21 mRNA levels were reduced, whereas SDF-1 and CXCR4 expression was increased (Figure 3). In OA primary chondrocytes, expression of p21 is decreased and phosphorylation of STAT3 significantly increased (data not shown). Conclusions: Our results suggest that p21 in chondrocytes functions to maintain matrix synthesis by regulation of aggrecan and MMP-13 expression via STAT3 phosphorylation. Because p21 levels are reduced in OA chondrocytes, our data imply that stabilization of p21 may be a therapeutic strategy for OA treatment.
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