NGF-p75 signaling coordinates skeletal cell migration during bone repair.
NGF-p75 signaling coordinates skeletal cell migration during bone repair.
复制标题
神经生长因子-p75信号在骨修复过程中协调骨骼细胞迁移。
DOI：
10.1126/sciadv.abl5716
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发表时间：
2022-03-18
期刊：
影响因子：
13.6
通讯作者：
James AW
中科院分区：
文献类型：
--
作者：
Xu J;Li Z;Tower RJ;Negri S;Wang Y;Meyers CA;Sono T;Qin Q;Lu A;Xing X;McCarthy EF;Clemens TL;James AW
损伤后的骨再生由炎症信号启动，并与感觉神经纤维的浸润相关。人们认为这些事件共同协调血管生成和组织重编程，但将免疫信号与神经再支配和成骨耦合的机制尚不清楚。在此，我们发现神经生长因子（NGF）在颅骨损伤后表达，并通过驻留的间充质成骨前体细胞中的p75发出信号，影响它们迁移到受损组织中。髓样细胞中缺乏Ngf的小鼠表现出成骨前体细胞向损伤部位的迁移减少，从而导致骨愈合延迟。Pdgfra +成骨细胞前体细胞中缺乏p75的小鼠也出现了这些相同的特征。单细胞转录组学鉴定出在细胞迁移和免疫反应中可能具有作用的间充质亚群，这些亚群在p75缺失的情况下发生改变。总之，这些结果确定了p75信号通路在早期骨修复过程中协调骨骼细胞迁移的作用。
通过p75信号的骨祖细胞迁移是颅骨正常修复中早期且必要的步骤。
Bone regeneration following injury is initiated by inflammatory signals and occurs in association with infiltration by sensory nerve fibers. Together, these events are believed to coordinate angiogenesis and tissue reprogramming, but the mechanism of coupling immune signals to reinnervation and osteogenesis is unknown. Here, we found that nerve growth factor (NGF) is expressed following cranial bone injury and signals via p75 in resident mesenchymal osteogenic precursors to affect their migration into the damaged tissue. Mice lacking Ngf in myeloid cells demonstrated reduced migration of osteogenic precursors to the injury site with consequently delayed bone healing. These features were phenocopied by mice lacking p75 in Pdgfra+ osteoblast precursors. Single-cell transcriptomics identified mesenchymal subpopulations with potential roles in cell migration and immune response, altered in the context of p75 deletion. Together, these results identify the role of p75 signaling pathway in coordinating skeletal cell migration during early bone repair. Osteoprogenitor cell migration via p75 signaling is an early and necessary step in proper calvarial bone repair.
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