Fig. 7: Graphical abstract.
From: Neutrophil-derived catecholamines mediate negative stress effects on bone
While mental trauma in general promotes bone marrow (BM) myelopoiesis, tyrosine hydroxylase (TH) expression and, consequently, the capacity to produce/ secrete catecholamines (CAs) is specifically facilitated in neutrophil granulocytes (NGRs). Neutrophil-derived CAs locally in the BM activate α/β-adrenoceptors (ARs) and dopaminergic receptors (DRs) on chondrocytes (CCs) and compromise their transdifferentiation into osteoblasts and, thus, bone metabolism. Neutrophil-derived CAs in an autocrine manner further promote their own BM emigration and, in case of a fracture, facilitate their own immigration into the fracture hematoma, likely in a paracrine manner by increasing CXCL1 release from hematoma mast cells and macrophages (MAs) which are two main CXCL1 producing cell types. In the fracture hematoma (FH), neutrophil-derived CAs again activate α/β-ARs and DA receptors on CCs and, consequently, compromise their transdifferentiation into osteoblasts (OBs) and, thus, adequate bone repair. (partly created with BioRender.com licensed to SOR). GP growth plate, TMD tissue mineral density, BV/TV bone volume/ tissue volume ratio, TB trabecular, GP growth plate, MPC myeloid progenitor cell, MO monocyte, RBA relative bone area, RCA relative cartilage area, RSTA relative soft tissue area, Oc.S/BS osteoclast surface/bone surface, N.Oc/ B.Pm number of osteoclasts/ bone perimeter.
