Single nuclei RNAseq of the bone fracture callus of Prss56-Nf1 KO mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA972647 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24557409.fastq.gz | Fastqsanger.gz | |||
| SRR24557410.fastq.gz | Fastqsanger.gz |
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Project description:Periosteum deficiency affects bone regeneration, especially in the case of the bone disorder congenital pseudarthrosis of the tibia (CPT). We investigated a new mouse model of CPT caused by Nf1 inactivation in boundary cap-derivatives, the Prss56Cre; R26tdTom; Nf1fl/fl model. To investigate altered healing in this CPT model, we generated a dataset of the injured periosteum and fracture callus at day-7 post fracture from Prss56Cre; R26tdTom; Nf1fl/fl mice.
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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.
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Project description:Skeletal stem/progenitor cells are critical for fracture repair by providing osteochondro precursors in the callus, which is impaired in aging. However, the molecular signatures of callus skeletan progenitor cells during aging is not known. We performed single-cell RNA sequencing on CD45-CD31-Ter119- skeletan progenitor cells isolated from young and aged mouse calluses.
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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.
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Project description:Interleukin-6 (IL-6) is highly upregulated in response to skeletal injury, suggesting it plays a role in the inflammatory phase of fracture repair. However, the impact of IL-6 on successful repair remains incompletely defined. Therefore, we investigated IL-6 in fracture repair using 12-week old IL-6 global knockout mice (IL-6 KO) and two models of fracture repair: full fracture and stress fracture. Callus formation 14 days after full fracture did not differ between IL-6 knockout mice and controls. However, IL-6 KO mice had an enhanced response 7 days after stress fracture compared to control, with increased callus (p=0.020) and bone formation (p=0.045). IL-6 KO did not alter the recruitment of neutrophils or macrophages to the stress fracture callus. IL-6 KO also did not alter the number of osteoclasts in the stress fracture callus. Based on RNA-seq, IL-6 KO resulted in only modest alterations to the gene expression at early time points after stress fracture. Wnt1 was more highly upregulated in IL-6 KO callus at both day 1 (fold change 12.5 vs. 5.7) and day 3 (fold change 4.7 vs. 1.9) compared to controls. Finally, using tibial compression to induce bone formation, we found that IL-6 KO directly impacted osteoblast function, increasing the propensity for woven bone formation. Herein, we report that IL-6 knockout enhanced formation of callus and bone following stress fracture injury, likely through direct action on the osteoblast’s ability to produce woven bone. This suggests a novel role of IL-6 as a suppressor of intramembranous bone formation.
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Project description:Fracture callus from young and aged mice
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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.
2013-11-27 | GSE45156 | GEO
Project description:Bone regeneration is a highly efficient process allowing scarless healing after injury. Yet, musculoskeletal traumatic injury, when fracture is combined with adjacent muscle injury, alters bone healing leading to fibrous nonunion. 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. We generated single nuclei datasets from the injured perioteum and hematoma at day 1-post fracture and from the hematoma/callus at day 5 post-musculoskeletal traumatic injury. These datasets were analyzed in combination with datasets from GSE234451.
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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.
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