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Rejuvenating aged osteoprogenitors for bone repair

ABSTRACT: To investigate cellular population heterogeneity, and gene expression in osteoprogenitors and other cell types (endothelial, osteogenic, immune) we isolate the calvarial periosteum and sagittal sutures as stem cell compartments that contribute to osteogenesis. We compare cell populations and gene expression between different ages of mouse, and also between different diets (ad libitum vs intermittent fasting)

ORGANISM(S): Mus musculus

PROVIDER: GSE226681 | GEO | 2024/12/06

REPOSITORIES: GEO

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Expansion of the sagittal suture induces proliferation of skeletal stem cells and sustains endogenous calvarial bone regeneration

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

Rejuvenating aged osteoprogenitors for bone repair

Project description:Rejuvenating aged osteoprogenitors for bone repair

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Comparative tissue gene expression profiling and alternative splicing by exon-sensitive microarrays in non-syndromic craniosynostosis

Project description:Craniosynostosis (CS) is the congenital premature fusion of one or more cranial sutures and represents the more prevalent craniofacial malformation in humans, with an overall incidence of 1 out of 2000-3000 live births. Non-syndromic craniosynostoses (NSC) are believed to be multifactorial disorders, with a strong genetic component, due to possible gene–gene or gene–environment interactions that remain to be clearly identified. In this study we delved into the molecular signaling acting in calvarial tissue and cells from patients affected by nonsynodromic midline craniosynostosis, using a comparative analysis between fused and unfused sutures of each affected individuals. Using comparative microarray tissue gene expression profiling we have identified a subset of genes involved in the structure and function of the primary cilium, including the Bardet-Biedl syndrome 9 (BBS9) gene, which was recently associated to sagittal synostosis in a GWAS study. We therefore characterized BBS9 expression and cilium-related signaling in cells isolated from patients’ calvarial bone.

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JUN induction in osteoprogenitors

Project description:Different osteoprogenitors (SSC, BCSP, Thy+) were sorted after 2 days of JUN induction, followed by RNA extraction and microarray analysis

2020-02-07 | GSE144829 | GEO

JUN induction in osteoprogenitors

Project description:JUN induction in osteoprogenitors

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A multi-stem cell basis for craniosynostosis and calvarial mineralization

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

Damaged Brain Accelerates Bone Healing by Releasing Exosomes that Target Osteoprogenitors

Project description:Clinical evidence has established that concomitant traumatic brain injury accelerates bone healing, but the underlying mechanism is unclear. This study showed that after TBI, injured neurons, mainly those in the hippocampus, released osteogenic microRNA (miRNA)-enriched exosomes, which targeted osteoprogenitors in bone to stimulate bone formation. Importantly, increased fibronectin expression on exosomal surface contributed to targeting of osteoprogenitors in bone by TBI exosomes, thereby implying that modification of the exosome surface fibronectin could be used in bone-targeted drug delivery. Together, our findings have established a novel role of central regulation in bone formation and a clear link between injured neurons and osteogenitors, both in animals and clinical settings.

2021-07-13 | PXD022126 | Pride

Prenatal dexamethasone exposure modificates H3K9me2 at the Mkp-1 locus in bone marrow osteoprogenitors

Project description:Prenatal dexamethasone exposure (PDE) has long-term consequences in bone development. we investigated how PDE exerts persistent effect on bone metabolism in mouse offspring. Our results showed that PDE offspring exhibited reduced bone mass, fewer osteoblasts and diminished osteoprogenitors proliferation.And PDE increased MKP-1 expression, while decreasing H3 lysine 9 dimethylation (H3K9me2) at Mkp-1 gene locus. Mechanistically, dexamethasone suppressed osteoprogenitors proliferation by upregulating MKP-1 expression, notably through the inhibition of H3K9me2 modifications, which promoted demethylation and transcriptional activation of the Mkp-1 gene. Importantly, restoring histone methylation balance with PFI-90 treatment blocked the inhibitory effects of PDE on MAPK signaling in osteoprogenitors, and mitigated the detrimental impact of PDE on osteoprogenitor proliferation and bone development in the offspring. Therefore,we performed ChIP-seq for H3K9me2 to identify its role in related epigenetic changes.

2024-11-06 | GSE276769 | GEO

Identification of adipo-osteoprogenitors in murine bone marrow

Project description:The bone marrow in mammals house both hematopoietic and mesenchymal cells that are responsible for sustaining blood and bone cell production, respectively, throughout adult life. Although the hematopoietic system is well understood, the molecular identities, hierarchy of the marrow mesenchymal cells and their respective contribution to bone homeostasis are just beginning to be unraveled. By employing single-cell RNA sequencing (scRNA-seq) technology, we have discovered a subset of bone marrow mesenchymal cells co-expressing adiponectin (Adipoq) and osterix (Osx) which are traditionally considered adipocyte or osteoblast markers, respectively. Trajectory analyses predict the Adipoq+Osx+ bi-marker cells to be common progenitors for osteoblasts and marrow adipogenic lineage cells. Lineage tracing with Osx-CreERT2 or Adipoq-CreERT2 supports that the bi-marker cells give rise to both osteoblasts and adipocytes in vivo. Imaging studies localize the bi-marker cells to the endosteal bone niche. The data therefore support the hypothesis that Adipoq+Osx+ bi-marker cells are adipo-osteoprogenitors attuned to the physiological milieu in the bone marrow. The studies have shed light on the role of the adipo- osteoprogenitors in bone physiology and pathophysiology.

2025-01-01 | GSE253262 | GEO

Runx2 regulates cranial suture closure by regulating hedgehog, Fgf, Wnt, and Pthlh signaling pathway genes in suture mesenchymal cells

Project description:CCD, which is characterized by hypoplastic clavicles, open fontanelles, supernumerary teeth, and short stature, are caused by heterozygous mutation of RUNX2. However, the reason why the suture closure is severely impaired in CCD patients remains to be clarified. The closure of posterior frontal (PF) and sagittal sutures was completely interrupted in Runx2+/– mice, and the proliferation of the suture mesenchymal cells was reduced compared with that in wild-type mice. To reveal the molecular mechanism, the differentially expressed genes between wild-type and Runx2+/– PF sutures were identified by microarray and real-time RT-PCR analyses. The expression of hedgehog, Fgf, Wnt, Pthlh signaling pathway genes, including Gli1, Ptch1, Ihh, Fgfr1-3, Tcf7, Wnt10b, Wnt1, and Pth1r, was reduced in PF sutures of Runx2+/– mice. These findings indicated that more than half dosage of Runx2 is required for the proliferation of suture mesenchymal cells, their commitment into osteoblast-lineage cells, and the induction of the hedgehog, Fgf, Wnt, and Pthlh signaling pathway gene expression in the sutures.

2019-10-09 | GSE119523 | GEO

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