These results identify a novel strategy for AC remediation via small molecule-mediated modulation of gp130 signalling.

Adenosine receptor A3 (A3) knockout results in progressive loss of articular cartilage in vivo. Ablation of A3 results in activation of matrix degradation and cartilage hypertrophy. A3 agonists downregulate RUNX2 and CaMKII expression in osteoarthritic human articular chondrocytes. A3 prevents articular cartilage matrix degradation induced by inflammation and osmotic fluctuations. A3 agonist inhibits proteolytic activity of cartilage-degrading enzymes.

Current study demonstrates a direct role for CaMKII in TGF-β and BMP-mediated responses in primary and PSC-derived chondrocytes. These findings have direct implications for tissue engineering of cartilage tissue from stem cells and therapeutic management of OA.

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CD4 þ cells can be sources of anti-inflammatory cytokines such as IL-4 and IL-10, as well as inhibiting the release of pro-inflammatory cytokines such as IL-1b or TNF-a. These findings support the notion that phenomena unrelated to long-term survival and engraftment of injected cells may have clear immunoregulatory effects.