| First Author | Meyers CA | Year | 2020 |
| Journal | Cell Rep | Volume | 31 |
| Issue | 8 | Pages | 107696 |
| PubMed ID | 32460020 | Mgi Jnum | J:304689 |
| Mgi Id | MGI:6514535 | Doi | 10.1016/j.celrep.2020.107696 |
| Citation | Meyers CA, et al. (2020) A Neurotrophic Mechanism Directs Sensory Nerve Transit in Cranial Bone. Cell Rep 31(8):107696 |
| abstractText | The flat bones of the skull are densely innervated during development, but little is known regarding their role during repair. We describe a neurotrophic mechanism that directs sensory nerve transit in the mouse calvaria. Patent cranial suture mesenchyme represents an NGF (nerve growth factor)-rich domain, in which sensory nerves transit. Experimental calvarial injury upregulates Ngf in an IL-1beta/TNF-alpha-rich defect niche, with consequent axonal ingrowth. In calvarial osteoblasts, IL-1beta and TNF-alpha stimulate Ngf and downstream NF-kappaB signaling. Locoregional deletion of Ngf delays defect site re-innervation and blunted repair. Genetic disruption of Ngf among LysM-expressing macrophages phenocopies these observations, whereas conditional knockout of Ngf among Pdgfra-expressing cells does not. Finally, inhibition of TrkA catalytic activity similarly delays re-innervation and repair. These results demonstrate an essential role of NGF-TrkA signaling in bone healing and implicate macrophage-derived NGF-induced ingrowth of skeletal sensory nerves as an important mediator of this repair. |
