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A Neurotrophic Mechanism Directs Sensory Nerve Transit in Cranial Bone.

Abstract：

: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-1β/TNF-α-rich defect niche, with consequent axonal ingrowth. In calvarial osteoblasts, IL-1β and TNF-α stimulate Ngf and downstream NF-κB 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.

journal_name

Cell Rep

journal_title

Cell reports

authors

Meyers CA,Lee S,Sono T,Xu J,Negri S,Tian Y,Wang Y,Li Z,Miller S,Chang L,Gao Y,Minichiello L,Clemens TL,James AW

doi

10.1016/j.celrep.2020.107696

subject

Has Abstract

pub_date

2020-05-26 00:00:00

pages

107696

issue

8

issn

2211-1247

pii

S2211-1247(20)30649-5

journal_volume

31

pub_type

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