Details

Autor(en) / Beteiligte

• Tschaffon-Müller, Miriam E A
• Kempter, Elena
• Steppe, Lena
• Kupfer, Sandra
• Kuhn, Melanie R
• Gebhard, Florian
• Pankratz, Carlos
• Kalbitz, Miriam
• Schütze, Konrad
• Gündel, Harald
• Kaleck, Nele
• Strauß, Gudrun
• Vacher, Jean
• Ichinose, Hiroshi
• Weimer, Katja
• Ignatius, Anita
• Haffner-Luntzer, Melanie
• Reber, Stefan O

Titel

Neutrophil-derived catecholamines mediate negative stress effects on bone

Ist Teil von

• Nature communications, 2023-06, Vol.14 (1), p.3262-3262, Article 3262

Ort / Verlag

England: Nature Publishing Group UK

Erscheinungsjahr

2023

Link zum Volltext

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• 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.