Abstract
Juvenile tissue healing is capable of extensive scarless healing that is distinct from the scar-forming process of the adult healing response. Although many growth factors can be found in the juvenile healing process, the molecular mechanisms of juvenile tissue healing are poorly understood. Here we show that juvenile mice deficient in the chemokine receptor CCR7 exhibit diminished large-scale healing potential, whereas CCR7-depleted adult mice undergo normal scar-forming healing similar to wild type mice. In addition, the CCR7 ligand CCL21 was transiently expressed around damaged cartilage in juvenile mice, whereas it is rarely expressed in adults. Notably, exogenous CCL21 administration to adults decreased scar-forming healing and enhanced hyaline-cartilage repair in rabbit osteochondral defects. Our data indicate that the CCL21/CCR7 axis may play a role in the molecular control mechanism of juvenile cartilage repair, raising the possibility that agents modulating the production of CCL21 in vivo can improve the quality of cartilage repair in adults. Such a strategy may prevent post-traumatic arthritis by mimicking the self-repair in juvenile individuals.
Highlights
Self-repair in juveniles is more extensive and scarless than in mature individuals[1]
Our findings demonstrate that the CCL21/CCR7 axis may constitute a part of the molecular control mechanism of juvenile cartilage repair, raising the possibility that agents modulating the production of CCL21 in vivo can improve the quality of cartilage repair in adults
CCL21 and CCR7 were detected in the bone marrow of adult wild type (WT) mice, they were largely absent at the injury site (Fig. 1D)
Summary
Self-repair in juveniles is more extensive and scarless than in mature individuals[1]. We have previously reported that cartilage tissues in adult mice showed low self-repair potential, whereas juvenile mice demonstrated hyaline-cartilage repair at the site of cartilage injury[3]. This suggests that clarifying the mechanisms of juvenile cartilage healing may improve the fate of adult cartilage injuries. Our findings demonstrate that the CCL21/CCR7 axis may constitute a part of the molecular control mechanism of juvenile cartilage repair, raising the possibility that agents modulating the production of CCL21 in vivo can improve the quality of cartilage repair in adults. This approach may have a great impact on cartilage repair therapy by mimicking self-repair in juveniles
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