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Myeloid-to-mesenchymal NGF-p75 signaling coordinates cell migration during repair.

ABSTRACT: Myeloid-to-mesenchymal NGF-p75 signaling coordinates cell migration during repair.

PROVIDER: PRJNA745466 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15097819_1.fastq.gz	Fastqsanger.gz
	SRR15097819_2.fastq.gz	Fastqsanger.gz
	SRR15097820_1.fastq.gz	Fastqsanger.gz
	SRR15097820_2.fastq.gz	Fastqsanger.gz
	SRR15097821_1.fastq.gz	Fastqsanger.gz

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Myeloid-to-mesenchymal NGF-p75 signaling coordinates cell migration during bone repair [scRNA-seq]

Project description:The cranial sutures are fibrous joints containing skeletal progenitor cells, which maintain homeostasis of the uninjured skull or participate in healing the skull after injury. Nerve growth factor (NGF) via its high-affinity receptor tropomyosin receptor kinase A (TrkA) regulates skeletal re-innervation, which is essential for later elements of bone repair, including revascularization and bone matrix deposition. However, emerging evidence suggests that NGF signaling may have more pleiotropic effects in bone repair than previously considered. In addition to induction of nerve ingrowth and promotion of nerve survival, pro-NGF may bind to its low-affinity receptor Ngfr (p75, Cd271), which is present in a variety of mesenchymal cells. p75 expression has been correlated to cell migration and invasion in multiple cell types. NGF binding to the p75 receptor stimulates migration and initiates recruitment of various adaptors, which activate NF-κB, RhoA, and c-Jun N-terminal kinase (JNK) signaling. In this study, single cell transcriptomics highlights altered signaling pathway activation and impaired cellular migration with p75 conditional gene deletion in PDGFRα-expressing cells.

2021-12-22 | GSE179890 | GEO

Myeloid-to-mesenchymal NGF-p75 signaling coordinates cell migration during bone repair [scRNA-seq]

Project description:Myeloid-to-mesenchymal NGF-p75 signaling coordinates cell migration during bone repair [scRNA-seq]

| PRJNA745469 | ENA

NGF-p75 signaling coordinates skeletal cell migration during bone repair.

Project description: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.

| S-EPMC8932666 | biostudies-literature

Expression data of mouse calvarial stem cells from p75 floxed mice (p75fl/fl) stimulated with Adenovirus encoding Cre recombinase (Ad-Cre) or control (Ad-GFP) [RNA-seq]

Project description:The cranial sutures are fibrous joints containing skeletal progenitor cells, which maintain homeostasis of the uninjured skull or participate in healing the skull after injury. Nerve growth factor (NGF) via its high-affinity receptor tropomyosin receptor kinase A (TrkA) regulates skeletal re-innervation, which is essential for later elements of bone repair, including revascularization and bone matrix deposition. However, emerging evidence suggests that NGF signaling may have more pleiotropic effects in bone repair than previously considered. In addition to induction of nerve ingrowth and promotion of nerve survival, pro-NGF may bind to its low-affinity receptor Ngfr (p75, Cd271), which is present in a variety of mesenchymal cells. p75 expression has been correlated to cell migration and invasion in multiple cell types. NGF binding to the p75 receptor stimulates migration and initiates recruitment of various adaptors, which activate NF-κB, RhoA, and c-Jun N-terminal kinase (JNK) signaling. In this study, changes in the transcriptome of calvarial stem cells after p75 knockout were evaluated by RNA sequencing.

2021-12-22 | GSE179889 | GEO

Myeloid-to-mesenchymal NGF-p75 signaling coordinates cell migration during repair.

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-12-22 | GSE179891 | GEO

β-NGF promotes cartilage to bone conversion, accelerating endochondral fracture repair

Project description:During endochondral fracture repair, a myriad of biochemical and phenotypic changes occur at the chondro-osseuous junction that regulate cartilage to bone conversion. Osteogenic and angiogenic factors have long been studied for accelerating fracture repair. In our concise study, we focused on the neurotrophic factor nerve growth factor (NGF) and its receptor tropomyosin receptor kinase A (TRKA) as understudied therapeutic targets for accelerating endochondral fracture repair. We first characterized endogenous expression of NGF and TRKA during endochondral repair of tibial fractures. We then analyzed gene expression data from β-NGF stimulated hypertrophic cartilage and observed a promotion in endochondral ossification associated markers. Additional gene ontology analyses revealed promotion of genes associated with Wnt activation, PDGF binding, and integrin binding. Subsequent histological analyses of in vivo samples confirmed Wnt activation following local β-NGF injections via reporter mice. Finally, we tested the therapeutic efficacy of local β-NGF injections in mice, which resulted in a decrease of cartilage and increase of bone volume. Moreover, the newly formed bone contained higher trabecular number, connective density, and bone mineral density. Collectively, we demonstrate the ability for β-NGF to promote endochondral fracture repair in a murine model and uncover mechanisms that will serve to further understand the molecular switches that occur during endochondral ossification.

2020-12-22 | GSE150092 | GEO

P75 neurotrophin receptor regulates BMP-induced SVZ neural stem cell migration.

Project description:P75 neurotrophin receptor regulates BMP-induced SVZ neural stem cell migration.

| PRJNA639162 | ENA

Transcription profiling of mouse Bax null versus NGF-Bax double null animals

Project description:We report that developmental competition between sympathetic neurons for survival is critically dependent on a sensitization process initiated by target innervation and mediated by a series of feedback loops. Target-derived nerve growth factor (NGF) promoted expression of its receptor TrkA in neurons and prolonged TrkA-mediated signals. NGF also controlled expression of brain derived neurotrophic factor (BDNF) and neurotrophin-4 (NT4), which, through the receptor p75, can kill neighboring neurons with low retrograde NGFâ??TrkA signaling whereas neurons with high NGFâ??TrkA signaling are protected. Perturbation of any of these feedback loops disrupts the dynamics of competition. We suggest that three target-initiated events are essential for rapid and robust competition between neurons: sensitization, paracrine apoptotic signaling, and protection from such effects. Experiment Overall Design: This experiment examine gene expression differences in superior cervical ganglia fro P0 bax null versus NGF-Bax double null animals. The Bax genotype was used in order to prevent the neuronal cell death normally observed in the NGF null animal.

2008-06-11 | E-GEOD-10498 | biostudies-arrayexpress

Comparison of SCG expression profiles from Bax null versus NGF-Bax double null mice

Project description:We report that developmental competition between sympathetic neurons for survival is critically dependent on a sensitization process initiated by target innervation and mediated by a series of feedback loops. Target-derived nerve growth factor (NGF) promoted expression of its receptor TrkA in neurons and prolonged TrkA-mediated signals. NGF also controlled expression of brain derived neurotrophic factor (BDNF) and neurotrophin-4 (NT4), which, through the receptor p75, can kill neighboring neurons with low retrograde NGF–TrkA signaling whereas neurons with high NGF–TrkA signaling are protected. Perturbation of any of these feedback loops disrupts the dynamics of competition. We suggest that three target-initiated events are essential for rapid and robust competition between neurons: sensitization, paracrine apoptotic signaling, and protection from such effects. Keywords: comparative gene expression analysis

2008-04-09 | GSE10498 | GEO

Olfactory Enshealting Cells : p75 High vs p75 Low cells population

Project description:Comparative gene expression profiling of olfactory enshealting cells : p75 High vs p75 Low cells population

2011-07-20 | GSE30797 | GEO