Neutrophil-derived catecholamines mediate negative stress effects on bone.
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
05 06 2023
05 06 2023
Historique:
received:
07
06
2022
accepted:
09
05
2023
medline:
7
6
2023
pubmed:
6
6
2023
entrez:
5
6
2023
Statut:
epublish
Résumé
Mental traumatization is associated with long-bone growth retardation, osteoporosis and increased fracture risk. We revealed earlier that mental trauma disturbs cartilage-to-bone transition during bone growth and repair in mice. Trauma increased tyrosine hydroxylase-expressing neutrophils in bone marrow and fracture callus. Here we show that tyrosine hydroxylase expression in the fracture hematoma of patients correlates positively with acknowledged stress, depression, and pain scores as well as individual ratings of healing-impairment and pain-perception post-fracture. Moreover, mice lacking tyrosine hydroxylase in myeloid cells are protected from chronic psychosocial stress-induced disturbance of bone growth and healing. Chondrocyte-specific β2-adrenoceptor-deficient mice are also protected from stress-induced bone growth retardation. In summary, our preclinical data identify locally secreted catecholamines in concert with β2-adrenoceptor signalling in chondrocytes as mediators of negative stress effects on bone growth and repair. Given our clinical data, these mechanistic insights seem to be of strong translational relevance.
Identifiants
pubmed: 37277336
doi: 10.1038/s41467-023-38616-0
pii: 10.1038/s41467-023-38616-0
pmc: PMC10241819
doi:
Substances chimiques
Catecholamines
0
Tyrosine 3-Monooxygenase
EC 1.14.16.2
Receptors, Adrenergic
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3262Informations de copyright
© 2023. The Author(s).
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