Murine fracture healing
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Winnie Liang
PROVIDER: E-GEOD-17825 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Time-point expression analysis of fractures calluses at 1, 3, and 5 days post-fracture in young and old BALB/c mice.
2009-09-01 | GSE17825 | GEO
Project description:mRNA gene expression was measured in intact female Sprague-Dawley rats at 6 (young), 26 (adult) and 52 (older) weeks of age at the time of fracture. Samples were collected at 0, 0.4, 1, 2, 4, and 6 weeks after fracture. RNA from two rats were pooled for each Affymetrix Rat U34A array. Mid-shaft, simple, transverse left femoral fractures were induced after retrograde intramedullary rod fixation with a Bonnarens and Einhorn device. Samples were collected from one third of the femoral length, centered on the fracture site, including the external callus, cortical bone, and marrow elements. Keywords = rat Keywords = fracture Keywords = age Keywords = time Keywords = femur Keywords: other
2004-01-10 | E-GEOD-594 | biostudies-arrayexpress
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
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.
2022-04-01 | GSE199755 | GEO
Project description:We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Geriatric fractures take longer to heal and heal with more complications than those of younger patients; however, the mechanistic basis for this difference in healing is not well understood. To improve this understanding, we investigated cell and molecular differences in fracture healing between 5 month-old (young adult) and 25 month-old (geriatric) mice healing utilizing high-throughput analysis of gene expression.
2018-01-01 | GSE99388 | GEO
Project description:Study of rat femur fracture healing in young (6 weeks old), adult (26 weeks old), and older (52 weeks old) rats with samples collected at 0 time (no fracture) and at 0.4, 1, 2, 4, and 6 weeks after fracture. RNA from two rats were pooled for each array. Keywords = rat, femur, fracture, age, time Keywords: time-course
2004-02-01 | GSE592 | GEO
Project description:mRNA gene expression was measured in intact female Sprague-Dawley rats at 6 (young), 26 (adult) and 52 (older) weeks of age at the time of fracture. Samples were collected at 0, 0.4, 1, 2, 4, and 6 weeks after fracture. RNA from two rats were pooled for each Affymetrix Rat U34A array. Mid-shaft, simple, transverse left femoral fractures were induced after retrograde intramedullary rod fixation with a Bonnarens and Einhorn device. Samples were collected from one third of the femoral length, centered on the fracture site, including the external callus, cortical bone, and marrow elements. Keywords = rat Keywords = fracture Keywords = age Keywords = time Keywords = femur Keywords: other
2004-01-10 | GSE594 | GEO
Project description:A study of rat femoral fracture healing in young (6 weeks old at fracture), adult (26 weeks old at fracture), and old (52 weeks old at fracture) rats. Samples were collected at time of surgery (intact controls) and at 3 days, 1 week, 2 weeks, 4 weeks, and 6 weeks after fracture. Samples were the mid third of the femoral length including the external callus, cortical bone and marrow elements. Fracture was stabilized with an intramedullary rod prior to fracture with a Bonnarens and Einhorn device. Keywords: time-course
2004-10-06 | GSE1371 | GEO
Project description:Phosphate is essential for healthy bone growth and plays an essential role in fracture repair. Although phosphate deficiency has been shown to impair fracture healing, the mechanisms involved in impaired healing are unknown. More recently, studies have shown that the effect of phosphate deficiency on the repair process varied based on the genetic strain of mice, which is not characterized. We used data from microarrays to (1) determine the effects of phosphate restriction on the biologic functions identified from the gene expression in fracture calluses; and (2) examine whether there are genetic differences within the primary biologic functions.
2018-12-25 | GSE99580 | GEO
Project description:HIF-1a activates genes under hypoxia and was hypothesized to regulate bone regeneration. Surprisingly, HET HIF-1a fracture calluses are larger, stronger and stiffer than WT HIF-1a calluses due to decreased apoptosis. These data identify apoptosis inhibition as a means to enhance bone regeneration. Introduction: Bone regeneration subsequent to fracture involves the synergistic activation of multiple signaling pathways. Localized hypoxia following fracture activates hypoxia-inducible factor 1 alpha (HIF-1a) leading to increased expression of HIF-1 target genes. We therefore hypothesized that HIF-1a is a key regulator of bone regeneration Materials and Methods: Fixed femoral fractures were generated in mice with partial HIF-1a deficiency (HET HIF-1a) and wild type littermates (WT HIF-1a). Fracture calluses and intact contralateral femurs from post fracture day (PFD) 21 and 28 (N=5-10) were subjected to MicroCT evaluation and 4-point bending in order to assess morphometric and mechanical properties. Molecular analyses were carried out on PFD 7, 10 and 14 samples (N=3) to determine differential gene expression at both mRNA and protein levels. Finally, TUNEL staining was performed on PFD 14 samples (N=2) to elucidate differential apoptosis. Results: Surprisingly, fracture calluses from HET HIF-1a mice exhibit greater mineralization and are larger, stronger and stiffer. Microarray analyses focused on hypoxia-induced genes revealed differential expression (between genotypes) of several genes associated with the apoptotic pathway. Real-time PCR confirmed these results, demonstrating higher expression of pro-apoptotic PP2A and lower expression of anti-apoptotic BCL2 in WT HIF-1a calluses. Subsequent TUNEL staining demonstrates that WT HIF-1a calluses contain larger numbers of TUNEL positive chondrocytes and osteoblasts than HET HIF-1a calluses. Conclusions: We conclude that partial HIF-1a deficiency results in decreased chondrocytic and osteoblastic apoptosis; thereby allowing the development of larger, stiffer calluses and enhancing bone regeneration. Furthermore, apoptosis inhibition may be a promising target for developing new treatments to accelerate bone regeneration. Keywords: Bone, Fracture, Apoptosis, Hypoxia, Microarray
2007-01-12 | GSE6091 | GEO