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Aged induced periosteal changes during early fracture healing

ABSTRACT: Aged induced periosteal changes during early fracture healing

PROVIDER: PRJNA1181030 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31199949_1.fastq.gz	Fastqsanger.gz
	SRR31199949_2.fastq.gz	Fastqsanger.gz
	SRR31199950_1.fastq.gz	Fastqsanger.gz
	SRR31199950_2.fastq.gz	Fastqsanger.gz
	SRR31199951_1.fastq.gz	Fastqsanger.gz

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Aged induced periosteal changes during early fracture healing

Project description:The periostieum is a fiberous network on the outside of the bones crucial to fracture healing. Here we present our scRNA-seq data from intact and fractured periosteal cells, collected three days after injury, from young adult and aged mice.

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Mechanosensitive Piezo1 is crucial for periosteal stem cell-mediated fracture healing

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YAP regulates periosteal expansion in early fracture repair.

Project description:Periosteal expansion is a key process in the early stages of bone fracture repair. The periosteum is typically quiescent, but upon fracture it expands, periosteal cells proliferate and contribute to the formation of a cartilaginous callus . The early expansion of the periosteum is tightly regulated at the transcriptional level. However, the molecular mechanisms behind periosteal expansion are unknown. Here, we show that Yes-Associated Protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) mediate periosteal expansion and periosteal cell proliferation. Bone fracture results in increased numbers of YAP-expressing periosteal cells. Deletion of YAP from Osterix (Osx) expressing periosteal cells impairs early periosteal expansion. Mechanistically, YAP regulates both cell intrinsic and extrinsic transcriptional programs that allow for periosteal expansion. Specifically, we identified Bmp4 as a cell extrinsic factor regulated by YAP, that rescues the impairment of periosteal expansion upon YAP deletion. Together, these data establish YAP mediated molecular mechanisms that allow for periosteal expansion in the early stages of fracture repair.

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Enabling adenosine signaling to promote aged fracture healing

Project description:Despite its regenerative capacity, the healing potential of bone tissue declines with aging. With the increase in global aging population, bone fractures pose a tremendous burden to the healthcare system. Therapeutic interventions that circumvent age-associated impairments and promote bone tissue regeneration are attractive options for geriatric fracture repair. We and others have demonstrated the role of extracellular adenosine in bone homeostasis and regeneration. Herein, we examined the changes in extracellular adenosine with aging and the potential of local delivery of adenosine to promote fracture healing using aged mice as a model system. Extracellular adenosine level was significantly lower in aged bone tissue compared to those from young mice. Concomitantly, the ecto-5′-nucleotidase CD73 expression was also found to be lower in the aged bone tissue. Local delivery of adenosine using injectable, in situ curing microgel delivery units yielded a pro-regenerative environment and promoted fracture healing in aged mice. This study offers new insights into age-related physiological changes in adenosine levels and demonstrates the therapeutic potential of adenosine supplementation to circumvent the compromised healing of geriatric fractures.

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Project description:Aged skeletal stem cells during fracture healing

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Enabling adenosine signaling to promote aged fracture healing

Project description:Enabling adenosine signaling to promote aged fracture healing

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Mechanosensitive Piezo1 is crucial for periosteal stem cell-mediated fracture healing

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Fracture healing in osteoporotic mice

Project description:Genome-wide comparative gene expression analysis of callus tissue of osteoporotic mice (Col1a1-Krm2 and Lrp5-/-) and wild-type were performed to identify candidate genes that might be responsible for the impaired fracture healing observed in Col1a1-Krm2 and Lrp5-/- mice. To investigate bone healing in osteoporosis, we performed fracture healing studies in wild-type mice (C57BL/6 genetic background) and the low bone mass strains Col1a1-Krm2 and Lrp5-/- (Schulze et al., 2010; Kato et al., 2002). Osteotomy was set in femora of female mice and stabilized by a semi-rigid fixator to allow fast bone healing (RM-CM-6ntgen et al., 2010). 21 days post surgery we analyzed the fracture calli by biochemical/histological methods, as well as micro-computed tomography, and observed impaired fracture healing in Col1a1-Krm2 and Lrp5-/- mice in comparison to wild-type. To identify genes that may be responsible for the impaired healing in osteoporotic mice, we performed microarray analysis of three independent callus samples of each genotype. The callus tissue was taken 10 days after surgery, because extensive bone formation took place at this point.

2013-10-25 | E-GEOD-51686 | biostudies-arrayexpress

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Project description:Fracture healing is a process that involves many cell populations. In this study we characterized gene expression in a subset of cells involved in fracture healing. αSMACreERT2 mice crossed with Ai9 reporter mice that express tdTomato fluorescent protein after Cre-mediated activation were used as an experimental model. αSMA-expressing cells were labeled by tamoxifen administration, then periosteal cells from the tibia were isolated two days later (controls), or tibial fractures were performed and periosteum/soft callus tissue was collected after 2 and 6 days. The tdTomato positive cell population was isolated by flow cytometry, and subjected to microarray analysis. Histology and cell surface marker analysis indicates that αSMACreERT2 labels a mainly mesenchymal population in the periosteum that expands after fracture, and contributes to both osteogenic and chondrogenic elements of the fracture callus. We were therefore able to examine gene expression in a defined population during the early stages of fracture healing. Total RNA was obtained from the tomato positive cells within the periosteal compartment of fractures from αSMACreERT2/Ai9 mice. Control animals were given 2 doses of tamoxifen, and periosteum was collected and labeled cells sorted (8-9 sex-matched mice per group). Fractures were performed after the second dose of tamoxifen, and tomato positive cells from periosteum/callus tissue were isolated 2 and 6 days after fracture (4-8 animals per sample pooled). 3 replicates for each sample are included.

2013-11-27 | E-GEOD-45156 | biostudies-arrayexpress

Single nuclei RNAseq of the periosteal response to bone fracture in mice

Project description:Bone regeneration is a highly efficient process allowing scarless healing after injury. The periosteum, the outer layer of bones, is a critical source of skeletal stem/progenitor cells (SSPCs), as well as immune, endothelial and neural cells during bone repair. In our study, we generated a single-nuclei atlas of the murine periosteal response to bone fracture. We generated single nuclei datasets from uninjured periosteum and from injured periosteum and hematoma/fracture callus at days 5 and 7 post-injury from wild-type mice.

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