Cellular Decoding of Simultaneous Cranial Mesenchyme and Osseous Architecture Reconstruction by Scaffolds
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE249260 | GEO | 2023/12/07
REPOSITORIES: GEO
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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.
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Project description:The regeneration of craniofacial bones of the mammalian skeleton necessitates the action of both intrinsic and extrinsic inductive factors from multiple cell types, which function in a hierarchical and temporal fashion to control the differentiation of osteogenic progenitors. Single-cell transcriptomics of developing mouse cranial suture recently identified a suture mesenchymal progenitor population with tendon- or ligament-associated gene expression profile previously uncharacterized. Here, we developed a Mohawk homeobox (MkxCG;R26RtdT) reporter mouse, finding that this teno-ligamentous gene identifies a cranial suture resident cell population within the adult mouse that gives rise to calvarial osteoblasts and osteocytes overtime during homeostatic conditions. Single cell RNA-Sequencing (scRNA-Seq) demonstrated that Mkx+ suture cells demonstrate a stem-like phenotype with expression of teno-ligamentous genes. Bone injury with Mkx+ cell ablation showed delayed bone healing. Remarkably, Mkx gene played a critical role as an osteo-inhibitory factor in cranial suture cells, as knockdown or knockout resulted in increased osteogenic differentiation. Furthermore, in vivo local deletion of Mkx in Mkx floxed mice resulted in robustly increased calvarial defect repair. Finally, we observed that mechanical stretch dynamically regulates Mkx expression in turn regulating calvarial cell osteogenesis. Overall, we identify Mkx+ cells within the suture mesenchyme as a progenitor cell population for adult craniofacial bones required for bone repair and Mkx itself as mechanical stretch responsive gene which functions to prevent osteogenic differentiation within the stem cell niche.
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Project description:The regeneration of craniofacial bones of the mammalian skeleton necessitates the action of both intrinsic and extrinsic inductive factors from multiple cell types, which function in a hierarchical and temporal fashion to control the differentiation of osteogenic progenitors. Single-cell transcriptomics of developing mouse cranial suture recently identified a suture mesenchymal progenitor population with tendon- or ligament-associated gene expression profile previously uncharacterized. Here, we developed a Mohawk homeobox (MkxCG;R26RtdT) reporter mouse, finding that this teno-ligamentous gene identifies a cranial suture resident cell population within the adult mouse that gives rise to calvarial osteoblasts and osteocytes overtime during homeostatic conditions. Single cell RNA-Sequencing (scRNA-Seq) demonstrated that Mkx+ suture cells demonstrate a stem-like phenotype with expression of teno-ligamentous genes. Bone injury with Mkx+ cell ablation showed delayed bone healing. Remarkably, Mkx gene played a critical role as an osteo-inhibitory factor in cranial suture cells, as knockdown or knockout resulted in increased osteogenic differentiation. Furthermore, in vivo local deletion of Mkx in Mkx floxed mice resulted in robustly increased calvarial defect repair. Finally, we observed that mechanical stretch dynamically regulates Mkx expression in turn regulating calvarial cell osteogenesis. Overall, we identify Mkx+ cells within the suture mesenchyme as a progenitor cell population for adult craniofacial bones required for bone repair and Mkx itself as mechanical stretch responsive gene which functions to prevent osteogenic differentiation within the stem cell niche.
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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.
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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.
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