Expression data from mouse calvarial suture mesenchymal cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE74849 | GEO | 2015/11/11
SECONDARY ACCESSION(S): PRJNA301674
REPOSITORIES: GEO
Similar Datasets
Project description:Axin2-expressing calvarial suture stem cells can contribute to calvarial development, homeostatic maintenance, repair, and regeneration. We used microarray to examine the gene expression profiles of Axin2-expressing suture stem cells and Axin2-negative cells in suture mesenchyme. Three of Axin2+/GFP+ and three of Axin2-/GFP- cell samples were collected from mice carrying Axin2rtTA and TREH2BGFP transgenes. Each samples were isolated from 6-8 Axin2rtTA; TRE-H2BGFP mice and sorted by the GFP intensity.
2015-11-11 | E-GEOD-74849 | biostudies-arrayexpress
Project description:Craniofacial development depends on formation and maintenance of sutures between bones of the skull. In sutures, growth occurs at osteogenic fronts along the edge of each bone and suture mesenchyme separates adjacent bones. We performed single-cell RNA-seq analysis of the embryonic, murine coronal suture. Seven populations at E16.5 and nine at E18.5 comprised the suture mesenchyme, osteogenic cells, and associated populations. Expression of Hhip, an inhibitor of hedgehog (HH) signaling, marked a mesenchymal population distinct from other neurocranial sutures. At E18.5, Hhip-/- coronal osteogenic fronts were closely apposed and HH signaling was increased throughout the depleted suture mesenchyme compared to WT, demonstrating that Hhip is required for normal coronal suture development. Tracing of the neonatal Hhip-expressing population showed that descendant cells persisted in the coronal suture and contributed to calvarial bone growth. Our transcriptomic approach provides a rich resource for insight into normal and abnormal development.
2021-06-26 | GSE178899 | GEO
Project description:Purpose: The cranial suture is a fibrous joint, and similar to the growth plates of the skeletal long bone, they serve as the major centers of calvarial vault morphogenesis. Our group’s identification of a skeletal stem cell isolated from the mouse tibial growth plate prompted us to investigate whether these skeletal stem cells are also resident in the mouse cranial sutures and if they govern postnatal suture patency or fusion. Results: We preformed a spatio-temporal profiling of the mouse cranial sutures by flow cytometry, demonstrating a significant decrease in the temporal representation of skeletal stem cells in fusing versus patent sutures. Moreover, canonical Wnt signaling has a significant impact on skeletal stem cells proliferation and thus representation within the suture, dictating fate: fusion or patency. Breeding an Axin2+/-LacZ mouse, with enhanced activation of canonical Wnt signaling to a Twist1+/− mouse, harboring a coronal craniosynostosis enriched the skeletal stem cell pool in coronal sutures, thereby preventing Twist1+/− craniosynostosis. Conclusions: Our findings suggest an imbalance and/or decrease in resident skeletal stem cells within the cranial sutures gives rise to craniosynostosis, however, restoring this representation by enriching skeletal stem cells within the suture can maintain patency.
2020-04-15 | GSE138881 | GEO
Project description:Purpose: The cranial suture is a fibrous joint, and similar to the growth plates of the skeletal long bone, they serve as the major centers of calvarial vault morphogenesis. Our group’s identification of a skeletal stem cell isolated from the mouse tibial growth plate prompted us to investigate whether these skeletal stem cells are also resident in the mouse cranial sutures and if they govern postnatal suture patency or fusion. Results: We preformed a spatio-temporal profiling of the mouse cranial sutures by flow cytometry, demonstrating a significant decrease in the temporal representation of skeletal stem cells in fusing versus patent sutures. Moreover, canonical Wnt signaling has a significant impact on skeletal stem cells proliferation and thus representation within the suture, dictating fate: fusion or patency. Breeding an Axin2+/-LacZ mouse, with enhanced activation of canonical Wnt signaling to a Twist1+/− mouse, harboring a coronal craniosynostosis enriched the skeletal stem cell pool in coronal sutures, thereby preventing Twist1+/− craniosynostosis. Conclusions: Our findings suggest an imbalance and/or decrease in resident skeletal stem cells within the cranial sutures gives rise to craniosynostosis, however, restoring this representation by enriching skeletal stem cells within the suture can maintain patency.
2020-04-15 | GSE138880 | GEO
Project description:In newborn humans, and up to approximately 2 y of age, calvarial bone defects can naturally regenerate. This remarkable regeneration potential is also found in newborn mice and is absent in adult mice. Since previous studies showed that the mouse calvarial sutures are reservoirs of calvarial skeletal stem cells (cSSCs), which are the cells responsible for calvarial bone regeneration, here we hypothesized that the regenerative potential of the newborn mouse calvaria is due to a significant amount of cSSCs present in the newborn expanding sutures. Thus, we tested whether such regenerative potential can be reverse engineered in adult mice by artificially inducing an increase of the cSSCs resident within the adult calvarial sutures.First, we analyzed the cellular composition of the calvarial sutures in newborn and in older mice, up to 14-mo-old mice, showing that the sutures of the younger mice are enriched in cSSCs. Then, we demonstrated that a controlled mechanical expansion of the functionally closed sagittal sutures of adult mice induces a significant increase of the cSSCs. Finally, we showed that if a calvarial critical size bone defect is created simultaneously to the mechanical expansion of the sagittal suture, it fully regenerates without the need for additional therapeutic aids. Using a genetic blockade system, we further demonstrate that this endogenous regeneration is mediated by the canonical Wnt signaling.This study shows that controlled mechanical forces can harness the cSSCs and induce calvarial bone regeneration. Similar harnessing strategies may be used to develop novel and more effective bone regeneration autotherapies.
2023-04-11 | GSE227468 | GEO
Project description:Sutures separate the flat bones of the skull and enable coordinated growth of the brain and overlying cranium. In order to uncover the cellular diversity within sutures, we conducted single-cell transcriptomic and histological analyses of the embryonic murine coronal suture. We identify Erg and Pthlh as early markers of osteogenic progenitors in sutures, and distinct pre-osteoblast signatures between the bone fronts and periosteum. diverse mesenchymal layers at the coronal suture, including multiple distinct meningeal layers below the suture, and ligamentous, ectocranial, and hypodermal layers above the sutureIn the ectocranial layers above the suture, we observe a ligament-like population spanning the frontal and parietal bones and expressing genes implicated in mechanosensation. Mesenchyme in and around the coronal suture is asymmetrically distributed between the frontal and parietal bones, and we identify different states of osteogenic cells extending from the bone fronts into the more mature bone, and a potential signature for sutural stem cellsIn the meningeal layers, we detect a potential chondrogenic periosteal dura population that may be involved in endochondral ossification that closes sutures. Expression of genes mutated in craniosynostosis is spread across diverse cell types, suggesting multiple points at which homeostasis can fail. This single-cell atlas provides a resource to understand the development of the coronal suture, the suture most commonly fused in craniosynostosis.
2021-06-17 | GSE163693 | GEO
Project description:Suture mesenchymal stem cell (MSC) drives calvarial suture development, homeostasis, and regeneration. Its loss leads to craniosynostosis, a prevailing craniofacial disorder characterized by premature suture closure. Ribosome biogenesis, historically thought to be a static house-keeping process, is now known to have tissue-specific roles. However, the functional specificity of ribosome biogenesis in suture MSCs remains largely unexplored, hampering development of therapeutic strategies for craniofacial tissue regeneration. We genetically perturb ribosome biogenesis using Snord118, a small nucleolar RNA (snoRNA) required for ribosomal RNA (rRNA) maturation. MSC specific conditional knockout (cKO) of Snord118 in mice leads to p53 activation, cell death, mesenchymal and MSC loss, impaired osteogenic and osteoclastic activity, resulting in suture growth and craniosynostosis defects. Using our newly established human induced pluripotent stem cell (iPSC)-derived MSCs combined with ribosome profiling, we found that SNORD118deficiency in MSCs causes global translation dysregulations and downregulation of complement pathway, a part of innate immune system with selective but poorly characterized physiological functions in craniofacial tissue homeostasis. Overall, ribosome biogenesis controls suture MSC fate via selective regulation of complement pathway.
2023-12-20 | GSE223615 | GEO
Project description:Suture mesenchymal stem cell (MSC) drives calvarial suture development, homeostasis, and regeneration. Its loss leads to craniosynostosis, a prevailing craniofacial disorder characterized by premature suture closure. Ribosome biogenesis, historically thought to be a static house-keeping process, is now known to have tissue-specific roles. However, the functional specificity of ribosome biogenesis in suture MSCs remains largely unexplored, hampering development of therapeutic strategies for craniofacial tissue regeneration. We genetically perturb ribosome biogenesis using Snord118, a small nucleolar RNA (snoRNA) required for ribosomal RNA (rRNA) maturation. MSC specific conditional knockout (cKO) of Snord118 in mice leads to p53 activation, cell death, mesenchymal and MSC loss, impaired osteogenic and osteoclastic activity, resulting in suture growth and craniosynostosis defects. Using our newly established human induced pluripotent stem cell (iPSC)-derived MSCs combined with ribosome profiling, we found that SNORD118deficiency in MSCs causes global translation dysregulations and downregulation of complement pathway, a part of innate immune system with selective but poorly characterized physiological functions in craniofacial tissue homeostasis. Overall, ribosome biogenesis controls suture MSC fate via selective regulation of complement pathway.
2023-12-20 | GSE223614 | GEO
Project description:The patterning and ossification of the mammalian skeleton requires the coordinated actions of both intrinsic bone morphogens and extrinsic neurovascular signals, which function in a temporal and spatial fashion to control mesenchymal progenitor cell (MPC) fate. Here we show genetic inhibition of Tropomyosin receptor kinase A (TrkA) sensory nerve innervation of the developing cranium results in premature calvarial suture closure, associated with a decrease in suture MPC proliferation. In vitro, axons from peripheral afferent neurons derived from DRGs of wild type mice induce MPC proliferation in a spatially-restricted manner via a soluble factor when co-cultured in microfluidic chambers. Comparative spatial transcriptomic analysis of the cranial sutures in vivo confirmed a positive association between sensory axons and proliferative MPCs. SpatialTime analysis across the developing suture revealed regional-specific alterations in BMP and TGFβ signaling pathway transcripts in response to TrkA inhibition. RNA sequencing of DRG cell bodies following direct axonal co-culture with MPCs confirmed alterations in BMP/TGFβ signaling pathway transcripts. Among these, the BMP inhibitor FSTL1 (Follistatin-like 1) replicated key features of the neural-to-bone influence, including mitogenic and anti-osteogenic effects via inhibition of BMP/TGFβ signaling. Taken together, our results demonstrate that sensory nerve-derived signals, including FSTL1, function to coordinate cranial bone patterning by regulating MPC proliferation and differentiation in the suture mesenchyme.
2021-09-29 | GSE174313 | GEO
Project description:FACS-sorted 2 bulk cell populations from mouse calvarial sutures (P7) were subjected to RNA sequencing. The samples were CTSK+ calvarial stem cells (labeled as PSC here) and DDR2+ calvarial stem cells isolated from CTSK-Cre;mTmG mice (n=5). The aim of this study was to obtain differentially expressed gene list for two different cell types as well as compare transcriptional profile between these populations.
2023-05-21 | GSE232652 | GEO