Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA631146 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11731535.fastq.gz	Fastqsanger.gz
	SRR11731536.fastq.gz	Fastqsanger.gz
	SRR11731537.fastq.gz	Fastqsanger.gz
	SRR11731538.fastq.gz	Fastqsanger.gz
	SRR11731539.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

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

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

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

| PRJNA631146 | ENA

Mesenchymal cell-derived septoclasts resorb cartilage during endochondral ossification and fracture healing

Project description:Mesenchymal cell-derived septoclasts resorb cartilage during endochondral ossification and fracture healing

2021-12-11 | GSE154076 | GEO

Transcriptional profiling of intramembranous and endochondral ossification after fracture in mice

Project description:Bone fracture repair represents an important clinical challenge with nearly 1 million non-union fractures occurring annually in the U.S. Gene expression differs between non-union and healthy repair, suggesting there is a pattern of gene expression that is indicative of optimal repair. Despite this, the gene expression profile of fracture repair remains incompletely understood. In this work, we used RNA-seq of two well-established murine fracture models to describe gene expression of intramembranous and endochondral bone formation. We used top differentially expressed genes, enriched gene ontology terms and pathways, callus cellular phenotyping, and histology to describe and contrast these bone formation processes across time. Intramembranous repair, as modeled by ulnar stress fracture, and endochondral repair, as modeled by femur full fracture, exhibited vastly different transcriptional profiles throughout repair. Stress fracture healing had enriched differentially expressed genes associated with bone repair and osteoblasts, highlighting the strong osteogenic repair process of this model. Interestingly, the PI3K-Akt signaling pathway was one of only a few pathways uniquely enriched in stress fracture repair. Full fracture repair involved a higher level of inflammatory and immune cell related genes than did stress fracture repair. Full fracture repair also differed from stress fracture in a robust downregulation of ion channel genes following injury, the role of which in fracture repair is unclear. This study offers a broad description of gene expression in intramembranous and endochondral ossification across several time points throughout repair and suggests several potentially intriguing genes, pathways, and cells whose role in fracture repair requires further study

2020-06-18 | GSE152677 | GEO

Local injections of β-NGF accelerates endochondral fracture repair by promoting cartilage to bone conversion.

Project description:There are currently no pharmacological approaches in fracture healing designed to therapeutically stimulate endochondral ossification. In this study, we test nerve growth factor (NGF) as an understudied therapeutic for fracture repair. We first characterized endogenous expression of Ngf and its receptor tropomyosin receptor kinase A (TrkA) during tibial fracture repair, finding that they peak during the cartilaginous phase. We then tested two injection regimens and found that local β-NGF injections during the endochondral/cartilaginous phase promoted osteogenic marker expression. Gene expression data from β-NGF stimulated cartilage callus explants show a promotion in markers associated with endochondral ossification such as Ihh, Alpl, and Sdf-1. Gene ontology enrichment analysis revealed the promotion of genes associated with Wnt activation, PDGF- and integrin-binding. Subsequent histological analysis confirmed Wnt activation following local β-NGF injections. Finally, we demonstrate functional improvements to bone healing following local β-NGF injections which resulted in a decrease in cartilage and increase of bone volume. Moreover, the newly formed bone contained higher trabecular number, connective density, and bone mineral density. Collectively, we demonstrate β-NGF's ability to promote endochondral repair in a murine model and uncover mechanisms that will serve to further understand the molecular switches that occur during cartilage to bone transformation.

| S-EPMC7747641 | biostudies-literature

Mesenchymal cell-derived septoclasts resorb cartilage during endochondral ossification and fracture healing

Project description:For scRNA-seq of fracture bone , 14 days post-fracture (PFD14) femur and control bones were harvested, cleaned surrounding tissue and the nail insert was removed from fracture bone. Control and PFD14 bone single cell suspension and non-hematopoietic stromal cells were prepared for scRNA-seq .

2021-12-10 | GSE154247 | GEO

Mesenchymal cell-derived septoclasts resorb cartilage during endochondral ossification and fracture healing

Project description:Mesenchymal cell-derived septoclasts resorb cartilage during endochondral ossification and fracture healing

| PRJNA645073 | ENA

Mesenchymal cell-derived septoclasts resorb cartilage during endochondral ossification and fracture healing

Project description:Mesenchymal cell-derived septoclasts resorb cartilage during endochondral ossification and fracture healing

| PRJNA645569 | ENA

Transcriptional profiling of intramembranous and endochondral ossification after fracture in mice

Project description:Transcriptional profiling of intramembranous and endochondral ossification after fracture in mice

| PRJNA640062 | ENA

Spatial transcriptomic analysis of a pre-clinical NF1 pseudarthrosis fracture model

Project description:Patients with Neurofibromatosis Type 1 (NF1) present with fracture pseudarthroses, though the exact mechanism underlying this abnormal healing remains unknown. Here, we performed spatial transcriptomics to spatially-define the molecular signatures across endochondral healing following fracture. Integrating single-cell sequencing of patient fracture-derived primary cells, our results provide a dynamic cellular context to the molecular dysregulation associated with somatic fracture healing defects in NF1.

2024-07-12 | GSE218046 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data