Skeletal Stem Cell Diversity in Mouse Long Bones
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA678366 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13058800_1.fastq.gz | Fastqsanger.gz | |||
| SRR13058800_2.fastq.gz | Fastqsanger.gz | |||
| SRR13058900_1.fastq.gz | Fastqsanger.gz | |||
| SRR13058900_2.fastq.gz | Fastqsanger.gz | |||
| SRR13059000_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 766 |
Similar Datasets
Project description:We have used SmartSeq2 to sequence single phenotypic skeletal stem cell (SSCs) populations purified via FACS from adult mouse long bones. Two putative SSC populations were isolated based on their previously reported surface marker profiles. An osteochondrogenic SSC (ocSSC, CD45-CD31-Tie2-Ter119-CD51+6C3-Thy1-CD105-) and a perivascular SSC (pvSSC, CD45-CD31-Pdgfra+Sca1+CD24+) were investigated.
2021-06-11 | GSE161477 | GEO
Project description:20 miRNAs were identified as differentially expressed in patients with infected nonunion of long bones, which may facilitate the diagnosis of infected nonunion of long bones.
2022-01-17 | GSE125289 | GEO
Project description:To identify specific markers for vertebral skeletal stem cells (vSSCs), we isolated vSSC candidates and lbSSCs by FACS from p10 mice long bone (tibia and femur) and vertebrae.
2023-05-05 | GSE230852 | GEO
Project description:Transcriptional profiling of long bone skeletal stem cells and vertebral counterparts
| PRJNA962848 | ENA
Project description:Mesenchymal stem cells (MSCs) And osteolineage cells contribute to the hematopoietic stem cell (HSC) Niche in the bone marrow of long bones. However, Their developmental relationships remain unclear. Here we demonstrate that different MSC populations in the developing marrow of long bones have distinct functions. Proliferative mesoderm-derived nestin- MSCs participate in fetal skeletogenesis, And lose MSC activity soon after birth. In contrast, Quiescent neural-crest-derived nestin+ Cells in the same bones preserve MSC activity, But do not generate fetal chondrocytes. Instead, They differentiate into HSC-niche-forming MSCs, Helping to establish the HSC niche by secreting Cxcl12. Perineural migration of these cells to the bone marrow requires the ErbB3 receptor. The neonatal Nestin-GFP+ PDGFR- Cell population also contains Schwann-cell precursors, But does not comprise mature Schwann cells. Thus, In the developing bone marrow HSC-niche-forming MSCs share a common origin with sympathetic peripheral neurons and glial cells, And ontogenically distinct MSCs have non-overlapping functions in endochondrogenesis and HSC niche formation. Total RNA was isolated from small numbers of FACS sorted stromal cells, obtained from neonatal Nes-Gfp bone marrow preparations (2 biological replicates). Each independent set of samples was obtained from pooled skeletal elements (long bones and sterna) form multiple littermates.
2014-10-15 | E-GEOD-61695 | biostudies-arrayexpress
Project description:The bone tissue undergoes constant turnover, which relies on skeletal stem cells (SSCs) and/or mesenchymal stem cells (MSCs) and their niches. SSCs/MSCs and their perivascular niche within the bone marrow are well characterized in long bones. As for cranial bones, besides bone marrow, the suture mesenchyme has been identified as a unique niche for SSCs/MSCs of craniofacial bones. However, a comprehensive study of the two different cranial stem cell niches at single-cell resolution is still lacking. In addition, during the progression of aging, age-associated changes in cranial stem cell niches and resident cells remain uncovered. In this study, we investigated age-related changes in cranial stem cell niches via single-cell RNA sequencing (scRNA-seq).
2023-09-11 | GSE235176 | GEO
Project description:Telomere shortening due to telomerase deficiency leads to accelerated senescence of human skeletal (mesenchymal) stem cells (MSC) in vitro. In order to study the role of telomere shortening in vivo, we studied the phenotype of telomerase deficient mice caused by absence of telomerase RNA component (TERC-/-). TERC-/- exhibited accelerated age-related bone loss starting at 3 months of age and during 12 months follow up. Bone histomorphometry revealed decreased mineralized surface and bone formation rate as well as increased osteoclast number and size in TERC-/-. Also, serum total deoxy-pyridinoline (tDPD) was increased in TERC-/-. MSC isolated from TERC-/- exhibited intrinsic defects with reduced total number, lower proliferation rate, decreased expression of osteoblastic (OB) differentiation markers and formed less in vivo ectopic bone compared to WT cells. The TERC-/--MSC cultures accumulated a larger proportion of senescent Ã-galactosidase+ cells and cells exhibiting DNA damage positive for γ-H2AX. Micro-array analysis of bones of TERC-/- and WT revealed significant over-expression of a large number of pro-inflammatory genes and signaling pathways in TERC-/- known to control osteoclast (OC) differentiation. In accordance with that, serum from TERC-/- enhanced OC formation in control bone marrow cultures. Our data demonstrate two mechanisms for age-related bone loss caused by telomerase deficiency: intrinsic osteoblastic defects and creation of pro-inflammatory osteoclast-activating microenvironment. Approaches for re-telomerization of MSC may provide a novel approach for abolishing age-related bone loss. control (WT) and the test (G3 - mTERC-/-) samples
2010-05-27 | E-GEOD-21523 | biostudies-arrayexpress
Project description:Skeletal aging and disease are associated with a misbalance in the opposing actions of osteoblasts and osteoclasts that are responsible for maintaining the integrity of bone tissues. Here, we show through detailed functional and single-cell genomic studies that intrinsic aging of bona fide mouse skeletal stem cells (SSCs) alters bone marrow niche signaling and skews bone and blood lineage differentiation leading to fragile bones that regenerate poorly. Aged SSCs have diminished bone and cartilage forming potential but produce higher frequencies of stromal lineages that express high levels of pro-inflammatory and pro-resorptive cytokines. Single-cell transcriptomic studies reveal a distinct population of SSCs in aged mice that gradually outcompete their younger counterparts in the bone marrow niche. While systemic exposure to a youthful circulation through heterochronic parabiosis reduced local expression of inflammatory cytokines, it did not reverse the diminished osteochondrogenic activity of aged SSCs and was insufficient to improve bone mass and skeletal-healing parameters in aged mice. Hematopoietic reconstitution of aged mice with young hematopoietic stem cells (HSC) also did not improve bone integrity and repair. We find that deficient bone regeneration in aged mice could only be reversed by the local application of a combinatorial treatment that re-activates aged SSCs and simultaneously abates crosstalk to hematopoietic cells favoring an inflammatory milieu. This treatment expanded aged SSC pools, reduced osteoclast activity, and enhanced bone healing to youthful levels. Our findings provide mechanistic insight into the complex, multifactorial mechanisms underlying skeletal aging and offer new prospects for rejuvenating the aged skeletal system.
2021-06-11 | GSE161946 | GEO
Project description:Skeletal aging and disease are associated with a misbalance in the opposing actions of osteoblasts and osteoclasts that are responsible for maintaining the integrity of bone tissues. Here, we show through detailed functional and single-cell genomic studies that intrinsic aging of bona fide mouse skeletal stem cells (SSCs) alters bone marrow niche signaling and skews bone and blood lineage differentiation leading to fragile bones that regenerate poorly. Aged SSCs have diminished bone and cartilage forming potential but produce higher frequencies of stromal lineages that express high levels of pro-inflammatory and pro-resorptive cytokines. Single-cell transcriptomic studies reveal a distinct population of SSCs in aged mice that gradually outcompete their younger counterparts in the bone marrow niche. While systemic exposure to a youthful circulation through heterochronic parabiosis reduced local expression of inflammatory cytokines, it did not reverse the diminished osteochondrogenic activity of aged SSCs and was insufficient to improve bone mass and skeletal-healing parameters in aged mice. Hematopoietic reconstitution of aged mice with young hematopoietic stem cells (HSC) also did not improve bone integrity and repair. We find that deficient bone regeneration in aged mice could only be reversed by the local application of a combinatorial treatment that re-activates aged SSCs and simultaneously abates crosstalk to hematopoietic cells favoring an inflammatory milieu. This treatment expanded aged SSC pools, reduced osteoclast activity, and enhanced bone healing to youthful levels. Our findings provide mechanistic insight into the complex, multifactorial mechanisms underlying skeletal aging and offer new prospects for rejuvenating the aged skeletal system.
2021-06-11 | GSE166441 | GEO