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Periosteal skeletal stem cells can migrate into the bone marrow and support hematopoiesis after injury

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE222272 | GEO | 2023/01/12

REPOSITORIES: GEO

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Periosteal skeletal stem cells can migrate into the bone marrow and support hematopoiesis after injury [I]

Project description:To investigate the transcriptomic differences between bone marrow mesenchymals stem cells and periosteal skeletal stem cells at steady state, and periosteal skeletal stem cells 72 hours after bone transplantation

2023-01-12 | GSE216824 | GEO

Periosteal skeletal stem cells can migrate into the bone marrow and support hematopoiesis after injury [II]

Project description:To investigate the transcriptomic differences between bone marrow mesenchymals stem cells and periosteal skeletal stem cells at steady state, and graft bone marrow mesenchymal stem cells 5 months after transplantation

2023-01-12 | GSE222271 | GEO

Periosteal skeletal stem cells can migrate into the bone marrow and support hematopoiesis after injury

Project description:Periosteal skeletal stem cells can migrate into the bone marrow and support hematopoiesis after injury

| PRJNA918732 | ENA

Periosteal skeletal stem cells can migrate into the bone marrow and support hematopoiesis after injury [II]

Project description:Periosteal skeletal stem cells can migrate into the bone marrow and support hematopoiesis after injury [II]

| PRJNA918733 | ENA

Periosteal skeletal stem cells can migrate into the bone marrow and support hematopoiesis after injury [I]

Project description:Periosteal skeletal stem cells can migrate into the bone marrow and support hematopoiesis after injury [I]

| PRJNA895452 | ENA

Comparative analysis of gene expression identifies distinct molecular signatures of bone marrow- and periosteal-skeletal stem/progenitor cells.

Project description:Periosteum and bone marrow (BM) both contain skeletal stem/progenitor cells (SSCs) that participate in fracture repair. However, the functional difference and selective regulatory mechanisms of SSCs in different locations are unknown due to the lack of specific markers. Here, we report a comprehensive gene expression analysis of bone marrow SSCs (BM-SSCs), periosteal SSCs (P-SSCs), and more differentiated osteoprogenitors by using reporter mice expressing Interferon-inducible Mx1 and NestinGFP, previously known SSC markers. We first defined that the BM-SSCs can be enriched by the combination of Mx1 and NestinGFP expression, while endogenous P-SSCs can be isolated by positive selection of Mx1, CD105 and CD140a (known SSC markers) combined with the negative selection of CD45, CD31, and osteocalcinGFP (a mature osteoblast marker). Comparative gene expression analysis with FACS-sorted BM-SSCs, P-SSCs, Osterix+ preosteoblasts, CD51+ stroma cells and CD45+ hematopoietic cells as controls revealed that BM-SSCs and P-SSCs have high similarity with few potential differences without statistical significance. We also found that CD51+ cells are highly heterogeneous and have little overlap with SSCs. This was further supported by the microarray cluster analysis, where the two SSC populations clustered together but are separate from the CD51+ cells. However, when comparing SSC population to controls, we found several genes that are uniquely upregulated in endogenous SSCs. Amongst these genes, we found KDR (aka Flk1 or VEGFR2) to be most interesting and discovered that it is highly and selectively expressed in P-SSCs. This finding suggests that endogenous P-SSCs are functionally very similar to BM-SSCs with undetectable significant differences in gene expression but there are distinct molecular signatures in P-SSCs, which can be useful to specify P-SSC subset in vivo.

| S-EPMC5771600 | biostudies-literature

Inflammatory signals from fatty bone marrow support DNMT3A driven clonal hematopoiesis.

Project description:Both fatty bone marrow (FBM) and somatic mutations in hematopoietic stem cells (HSCs), also termed clonal hematopoiesis (CH) accumulate with human aging. However it remains unclear whether FBM can modify the evolution of CH. To address this question, we herein present the interaction between CH and FBM in two preclinical male mouse models: after sub-lethal irradiation or after castration. An adipogenesis inhibitor (PPARγ inhibitor) is used in both models as a control. A significant increase in self-renewal can be detected in both human and rodent DNMT3AMut-HSCs when exposed to FBM. DNMT3AMut-HSCs derived from older mice interacting with FBM have even higher self-renewal in comparison to DNMT3AMut-HSCs derived from younger mice. Single cell RNA-sequencing on rodent HSCs after exposing them to FBM reveal a 6-10 fold increase in DNMT3AMut-HSCs and an activated inflammatory signaling. Cytokine analysis of BM fluid and BM derived adipocytes grown in vitro demonstrates an increased IL-6 levels under FBM conditions. Anti-IL-6 neutralizing antibodies significantly reduce the selective advantage of DNMT3AMut-HSCs exposed to FBM. Overall, paracrine FBM inflammatory signals promote DNMT3A-driven clonal hematopoiesis, which can be inhibited by blocking the IL-6 pathway.

| S-EPMC10097668 | biostudies-literature

Itm2a expression marks periosteal skeletal stem cells that contribute to bone fracture healing.

Project description:The periosteum contains skeletal stem/progenitor cells that contribute to bone fracture healing. However, the in vivo identity of periosteal skeletal stem cells (P-SSCs) remains unclear, and membrane protein markers of P-SSCs that facilitate tissue engineering are needed. Here, we identified integral membrane protein 2A (Itm2a) enriched in SSCs using single-cell transcriptomics. Itm2a+ P-SSCs displayed clonal multipotency and self-renewal and sat at the apex of their differentiation hierarchy. Lineage-tracing experiments showed that Itm2a selectively labeled the periosteum and that Itm2a+ cells were preferentially located in the outer fibrous layer of the periosteum. The Itm2a+ cells rarely expressed CD34 or Osx, but expressed periosteal markers such as Ctsk, CD51, PDGFRA, Sca1, and Gli1. Itm2a+ P-SSCs contributed to osteoblasts, chondrocytes, and marrow stromal cells upon injury. Genetic lineage tracing using dual recombinases showed that Itm2a and Prrx1 lineage cells generated spatially separated subsets of chondrocytes and osteoblasts during fracture healing. Bone morphogenetic protein 2 (Bmp2) deficiency or ablation of Itm2a+ P-SSCs resulted in defects in fracture healing. ITM2A+ P-SSCs were also present in the human periosteum. Thus, our study identified a membrane protein marker that labels P-SSCs, providing an attractive target for drug and cellular therapy for skeletal disorders.

| S-EPMC11364384 | biostudies-literature

Bone marrow Tregs mediate stromal cell function and support hematopoiesis via IL-10.

Project description:The nonimmune roles of Tregs have been described in various tissues, including the BM. In this study, we comprehensively phenotyped marrow Tregs, elucidating their key features and tissue-specific functions. We show that marrow Tregs are migratory and home back to the marrow. For trafficking, marrow Tregs use S1P gradients, and disruption of this axis allows for specific targeting of the marrow Treg pool. Following Treg depletion, the function and phenotype of both mesenchymal stromal cells (MSCs) and hematopoietic stem cells (HSCs) was impaired. Transplantation also revealed that a Treg-depleted niche has a reduced capacity to support hematopoiesis. Finally, we found that marrow Tregs are high producers of IL-10 and that Treg-secreted IL-10 has direct effects on MSC function. This is the first report to our knowledge revealing that Treg-secreted IL-10 is necessary for stromal cell maintenance, and our work outlines an alternative mechanism by which this cytokine regulates hematopoiesis.

| S-EPMC7710301 | biostudies-literature

Memory B lymphocytes migrate to bone marrow in humans.

Project description:IgM-bearing B lymphocytes with mature phenotype (CD10- CD24(lo) IgD+) are acquired after birth in the bone marrow of humans. These B cells are defined here as relatively large, nondividing lymphocytes, variable proportions of which express cell surface molecules indicative of relatively recent activation. Analysis of V(H)5(2) (heavy chain variable region) gene transcripts indicated point mutations throughout the Ig variable region from the mature IgM+ B population but not from the immature B cells in the bone marrow. The mutations were concentrated in the complementarity determining regions, and amino acid substitutions were favored over silent mutations, findings indicative of antigen selection within germinal centers in peripheral lymphoid tissues. The V(H) sequence analysis also revealed the existence of clonal relatives in individual bone marrow samples. These antigen-experienced lymphocytes did not secrete Ig spontaneously but could be induced to do so in vitro. The data suggest that a subpopulation of memory B lymphocytes generated during antigen responses recirculates to the bone marrow in humans.

| S-EPMC19286 | biostudies-literature

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