Expression data of PDGFRα- and PDGFRα+ mesenchymal stem cells isolated from mouse periosteum
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ABSTRACT:
PROVIDER: PRJNA644793 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12171530_1.fastq.gz | Fastqsanger.gz | |||
| SRR12171530_2.fastq.gz | Fastqsanger.gz | |||
| SRR12171531_1.fastq.gz | Fastqsanger.gz | |||
| SRR12171531_2.fastq.gz | Fastqsanger.gz | |||
| SRR12171532_1.fastq.gz | Fastqsanger.gz |
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Project description:The outer coverings of the skeleton, or periosteum, are arranged in concentric layers and act as a reservoir for tissue specific bone progenitors. Cellular heterogeneity within this tissue depot is increasingly recognized. Here, Pdgfra reporter animals were used to highlight a subset of periosteal progenitor cells with high osteogenic potential. Pdgfra+ periosteal progenitor cells enhanced osteogenic differentiation in vitro and improved fracture healing and bone regeneration in vivo. Depletion of Pdgfra-expressing progenitor cells interferes with cortical appositional bone, periosteal bone formation in response to mechanical load, and during fracture repair. Pdgfra+ periosteal progenitors give rise to Nestin+ periosteal cells overtime, after fracture and upon transplantation.
2022-02-02 | GSE154003 | GEO
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2022-05-26 | PXD023428 | Pride
Project description:Bone regeneration relies on the activation of skeletal stem cells (SSCs) that still remain poorly characterized. Here, we show that periosteum contains SSCs with high bone regenerative potential compared to bone marrow stromal cells/skeletal stem cells (BMSCs) in mice. Although periosteal cells (PCs) and BMSCs are derived from a common embryonic mesenchymal lineage, post-natally PCs exhibit greater clonogenicity, growth and differentiation capacity than BMSCs. During bone repair, PCs can efficiently contribute to cartilage and bone, and integrate long-term after transplantation. Molecular profiling uncovers genes encoding Periostin and other extracellular matrix molecules associated with the enhanced response to injury of PCs. Periostin gene deletion impairs PC functions and fracture consolidation. Periostin-deficient periosteum cannot reconstitute a pool of PCs after injury demonstrating the presence of SSCs within periosteum and the requirement of Periostin in maintaining this pool. Overall our results highlight the importance of analyzing periosteum and PCs to understand bone phenotypes.
2018-10-18 | E-MTAB-6417 | biostudies-arrayexpress
Project description:Periosteum is a major source of skeletal stem/progenitor cells (SSPCs) during bone repair. However, the cellular composition of the periosteum is poorly characterized. Here, we provide single-cell RNAseq data of periosteal cells isolated by explant culture at steady state and at day 3 post-tibial fracture. We found that periosteal cell populations are heterogeneous containing several sub-populations of SSPCs. Upon fracture, SSPCs are activated by leaving their mesenchymal state, and engaging into fibrogenesis prior to chondrogenesis.
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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:We utilized a fate-mapping approach to investigate alpha-smooth muscle actin (αSMA)+ and platelet derived growth factor-alpha (PDGFRα)+ cells in two lung fibrosis models, complemented by cell-type specific next-generation sequencing and investigations on human lungs. Our data revealed that αSMA+ and PDGFRα+ cells mark two distinct mesenchymal lineages with minimal transdifferention potential during lung fibrotic remodeling. Parenchymal and perivascular fibrotic regions were populated predominantly with PDGFRα+ cells expressing collagen, while αSMA+ cells in the parenchyma and vessel wall showed variable expression of collagen and the contractile protein desmin. The distinct gene expression profiles found in normal conditions was retained during pathologic remodeling. Cumulatively, our findings identify αSMA+ and PDGFRα+ cells as two separate lineages with distinct gene expression profile in adult lungs.
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Project description:PDGFRα+ cells are interstitial/perivascular mesenchymal progenitor cells that have been associated with fibro-adipogenic processes. However, their function during tissue homeostasis or in response to revascularization and regeneration stimuli remains to be fully defined. Here, by high-throughput transcriptomic analysis, adoptive transfer and multicolor lineage tracking we showed that PDGFRα+ cells from skeletal muscle cluster as a population that is transcriptionally distinct from other mesenchymal stromal cells and with an essential role in tissue revascularization and restructuring of ischemic areas. We further showed that tissue regeneration involves the removal of differentiated PDGFRα+-derived cells, while pathological healing occurred if PDGFRα+-derived cells persisted as terminally differentiated mesenchymal cells (e.g. myofibroblasts). From the perspective of tissue regeneration, these studies support a context-dependent 'yin-yang' biology of PDGFRα+ cells, that possess an innate ability to stabilize newly formed blood vessels and concurrently limit injury expansion after ischemia, while also being capable of promoting fibrosis in an unfavorable environment.
2019-07-01 | GSE101930 | GEO
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:Limb development begins with limb buds that develop into long appendicular bones separated by joint-forming structures called interzones. Mesenchymal progenitor cells of the interzone differentiate into cartilaginous and fibrous tissues of the synovial joint, including articular cartilage, menisci, and ligaments. Platelet-derived growth factor receptor-α (PDGFRα) is expressed by mesenchymal cells of the limb bud, but it is not known to have a role in limb or joint development. By analyzing PDGFRα expression in single-cell RNA sequencing data, immunofluorescence, and lineage tracing, we observed dynamic PDGFRα expression in the mouse limb bud, interzone, and perichondral mesenchyme. To investigate PDGFRα function, we use Prrx1-Cre to cause mouse limb bud mesenchyme to express mutant PDGFRα with a kinase domain point mutation (D842V) that increases receptor signaling. Overall limb development was unaffected. However, the hind limbs were immobile with knee joints fused by cartilage and lacking ligaments and menisci. The mutant perichondrium exhibited ectopic cartilage matrix and the enthesis of the patellar tendon was enlarged. The interzone marker Gdf5 was initially expressed at E12.5 but was downregulated at E13.5 and thereafter, suggesting a defect in maintenance of the interzone. Spatial transcriptomics of the mutant joint identified co-expression of genes for both cartilage (Sox9, Col2a1) and fibrotic tissue (Postn, Col1a1, Col1a2), suggesting fibrocartilage. These data suggest that elevated PDGFRα signaling corrupts joint tissue differentiation by downregulating Gdf5 and redirecting interzone progenitors into a fibrocartilage fate. These results highlight the need to balance chondrogenic and fibrogenic cell fates during joint development, with tight regulation of PDGFRα signaling as a necessity for the development of the mouse knee joint.
2025-04-01 | GSE289873 | GEO
Project description:The platelet-derived growth factor receptor alpha (PDGFRα) exhibits divergent effects in skeletal muscle. At physiological levels, signaling through this receptor promotes muscle development in growing embryos and proper angiogenesis in regenerating adult muscle. However, either increased PDGF ligands or enhanced PDGFRα pathway activity causes pathological fibrosis. This excessive collagen deposition, which is seen in aged and diseased muscle, interferes with proper muscle function and limits the effectiveness of gene- and cell-based therapies for muscle disorders. Although compelling evidence exists for the role of PDGFRα in fibrosis, little is known about the cells through which this pathway acts. Here we show that PDGFRα signaling regulates a population of muscle-resident fibro/adipogenic progenitors (FAPs) that play a supportive role in muscle regeneration but may also cause fibrosis when aberrantly regulated. We found that FAPs produce multiple transcriptional variants of PDGFRα with different polyadenylation sites, including an intronic variant that codes for a protein isoform containing a truncated kinase domain. This variant, upregulated during regeneration, acts as a decoy to inhibit PDGF signaling and to prevent FAP over-activation. Moreover, increasing expression of this isoform limits fibrosis in vivo, suggesting both biological relevance and therapeutic potential of modulating polyadenylation patterns in stem cell populations. We used microarrays to explore the biological effects of altering intronic polyadenylation of PDGFRα in FAPs.
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