CCL21/CCR7 axis regulating juvenile cartilage repair can enhance cartilage healing in adults.
Aging
/ metabolism
Animals
Bone and Bones
/ drug effects
Cartilage
/ drug effects
Cell Differentiation
/ drug effects
Cell Movement
/ drug effects
Cells, Cultured
Chemokine CCL21
/ administration & dosage
Chondrocytes
/ drug effects
Chondrogenesis
/ drug effects
Female
Mesenchymal Stem Cells
/ drug effects
Mice, Inbred C57BL
Rabbits
Receptors, CCR7
/ metabolism
Signal Transduction
Wound Healing
/ drug effects
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
26 03 2019
26 03 2019
Historique:
received:
08
03
2018
accepted:
14
03
2019
entrez:
28
3
2019
pubmed:
28
3
2019
medline:
2
10
2020
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 30914733
doi: 10.1038/s41598-019-41621-3
pii: 10.1038/s41598-019-41621-3
pmc: PMC6435673
doi:
Substances chimiques
Ccr7 protein, mouse
0
Chemokine CCL21
0
Receptors, CCR7
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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