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Alternate protein kinase A activity identifies a unique population of stromal cells in adult bone

ABSTRACT: We investigated the Prkar1a+/- mice when bred with Prkaca+/- genetic backgrounds. Prkar1a+/-Prkaca+/- mice not only continued to develop bone lesions but also demonstrated a significant increase in both the number and the severity of the lesions, as well as a reduction in the age of first appearance of any bone abnormality. Histological analysis of bone from Prkar1a+/-Prkaca+/- mice showed that lesions had similarity to tumors from humans with CNC and some resemblance (but also differences) from humans and mice with fibrous dysplasia (FD). Prkar1a+/- and Prkar1a+/-Prkaca+/- mouse lesions always involved a particular sub-population of cells that could be identified as belonging to the osteoblastic lineage, that were initially located on the endosteal surface of the periosteum and nearby trabecular bone proximal to the growth plate of the long bones and vertebrae, and resembled bone stromal cells (BSCs). The bone lesions expressed high level of mesenchymal proteins like n-cadherin, vimentin, snail1, twist1, mmp2 and mmp9 when compared to WT bone. On top of this, bone lesions from Prkar1a+/-Prkaca+/- mice also showed an increased expression of keratin related genes, which are involved in hair follicle and epithelial differentiation, when compared to lesions from Prkar1a+/- mice. Total RNA obtained from bone lesions from Prkar1a+/- and Prkar1a+/-Prkaca+/- mice were compared to those obtained from WT and Prkaca+/- mice.

ORGANISM(S): Mus musculus

SUBMITTER: C Cheadle

PROVIDER: E-GEOD-20984 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Alternate protein kinase A activity identifies a unique population of stromal cells in adult bone

Project description:We investigated the Prkar1a+/- mice when bred with Prkaca+/- genetic backgrounds. Prkar1a+/-Prkaca+/- mice not only continued to develop bone lesions but also demonstrated a significant increase in both the number and the severity of the lesions, as well as a reduction in the age of first appearance of any bone abnormality. Histological analysis of bone from Prkar1a+/-Prkaca+/- mice showed that lesions had similarity to tumors from humans with CNC and some resemblance (but also differences) from humans and mice with fibrous dysplasia (FD). Prkar1a+/- and Prkar1a+/-Prkaca+/- mouse lesions always involved a particular sub-population of cells that could be identified as belonging to the osteoblastic lineage, that were initially located on the endosteal surface of the periosteum and nearby trabecular bone proximal to the growth plate of the long bones and vertebrae, and resembled bone stromal cells (BSCs). The bone lesions expressed high level of mesenchymal proteins like n-cadherin, vimentin, snail1, twist1, mmp2 and mmp9 when compared to WT bone. On top of this, bone lesions from Prkar1a+/-Prkaca+/- mice also showed an increased expression of keratin related genes, which are involved in hair follicle and epithelial differentiation, when compared to lesions from Prkar1a+/- mice.

2010-03-21 | GSE20984 | GEO

Identify acetylation marks in adult mouse L4 vertebrae gene promoter regions from maternal high fat diet dams using H3K27ac ChIP-Seq

Project description:Genes with increased H3K27ac marks in their promoters were found in adult mice L4 vertebrae from mice using H3K27ac ChIP-Seq. Recent data suggests that in animals and humans that a maternal diet high in fat leads to poor bone growth and development in offspring. Genes with increased H3K27ac epigenetic marks normally have higher levels of expression. Understanding which genes are being upregulated due to maternal or offspring high fat diet would allow for better treatments to combat bone loss to be developed.

2022-05-31 | E-MTAB-11718 | biostudies-arrayexpress

Periosteum contains skeletal stem cells with high bone regenerative potential controlled by Periostin

Project description:Bone regeneration relies on the activation of skeletal stem cells (SSCs) that still remain poorly characterized. Here, we show that periosteum contains SSCs with high bone regenerative potential compared to bone marrow stromal cells/skeletal stem cells (BMSCs) in mice. Although periosteal cells (PCs) and BMSCs are derived from a common embryonic mesenchymal lineage, post-natally PCs exhibit greater clonogenicity, growth and differentiation capacity than BMSCs. During bone repair, PCs can efficiently contribute to cartilage and bone, and integrate long-term after transplantation. Molecular profiling uncovers genes encoding Periostin and other extracellular matrix molecules associated with the enhanced response to injury of PCs. Periostin gene deletion impairs PC functions and fracture consolidation. Periostin-deficient periosteum cannot reconstitute a pool of PCs after injury demonstrating the presence of SSCs within periosteum and the requirement of Periostin in maintaining this pool. Overall our results highlight the importance of analyzing periosteum and PCs to understand bone phenotypes.

2018-10-18 | E-MTAB-6417 | biostudies-arrayexpress

Prkar1a haploinsufficiency leads to an overall increase in tumors caused by other genetic defects or chemical induction

Project description:[original title] Prkar1a haploinsufficiency in mice leads to an overall increase in tumors caused by other genetic defects or chemical induction We investigated the Prkar1a+/- mice when bred within the Rb1+/- or Trp53+/- genetic backgrounds, or treated with a 2-step skin carcinogenesis protocol. Prkar1a+/-Trp53+/- mice developed more bone sarcomas than Trp53+/- mice (p<0.05) and Prkar1a+/-Rb1+/- mice grew more and larger pituitary and thyroid tumors than Rb1+/- mice. All mice with double heterozygosity had significantly reduced life-spans compared with their single-heterozygous counterparts. Finally, Prkar1a+/- mice developed more papillomas than wild-type animals when treated with a 2-step skin carcinogenesis protocol. A whole-genome transcriptome profiling of tumors produced by all three models identified Wnt signaling as the main pathway activated by abnormal cAMP signaling in these tissues, along with (expected) cell cycle gene abnormalities, all confirmed by qRT-PCR array and immunohistochemical analyses.

2009-12-24 | GSE19576 | GEO

Transcriptional profiling of EMB+ cells and EMB- cells across long bone and vertebrae

Project description:To compare gene expression profiling of EMB+ cells and EMB- cells whin CD45-Ter119-CD31--Thy1-6C3-CD200+CD105- population across long bone and vertebrae, we isolated related cells form long bone or vertebrae of zic1 -cre mtmg mice by FACS.

2023-04-30 | GSE230724 | GEO

Single nuclei RNAseq of the periosteal response to bone fracture in mice

Project description:Bone regeneration is a highly efficient process allowing scarless healing after injury. The periosteum, the outer layer of bones, is a critical source of skeletal stem/progenitor cells (SSPCs), as well as immune, endothelial and neural cells during bone repair. In our study, we generated a single-nuclei atlas of the murine periosteal response to bone fracture. We generated single nuclei datasets from uninjured periosteum and from injured periosteum and hematoma/fracture callus at days 5 and 7 post-injury from wild-type mice.

2024-04-01 | GSE234451 | GEO

Single nuclei RNAseq of the bone fracture callus of Prss56-Nf1 KO mice

Project description:Periosteum deficiency affects bone regeneration, especially in the case of the bone disorder congenital pseudarthrosis of the tibia (CPT). We investigated a new mouse model of CPT caused by Nf1 inactivation in boundary cap-derivatives, the Prss56Cre; R26tdTom; Nf1fl/fl model. To investigate altered healing in this CPT model, we generated a dataset of the injured periosteum and fracture callus at day-7 post fracture from Prss56Cre; R26tdTom; Nf1fl/fl mice.

2024-07-24 | GSE232517 | GEO

Gene expression profile of murine bone marrow endosteal populations

Project description:This SuperSeries is composed of the following subset Series: GSE17569: Gene expression profile of murine bone marrow endosteal populations (1) GSE17570: Gene expression profile of murine bone marrow endosteal populations (2) Refer to individual Series

2010-08-10 | E-GEOD-17597 | biostudies-arrayexpress

Transcriptional profiling of long bone skeletal stem cells and vertebral counterparts

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

Identification of LRP1 and CD13 expressing human periosteal cells for stem cell-mediated bone repair [human scRNA-seq]

Project description:Human periosteal skeletal stem cells (P-SSCs) are critical for cortical bone maintenance and repair. However, their in vivo identity, molecular characteristics, and specific markers remain unknown. Here, single-cell sequencing revealed human periosteum contains SSC clusters expressing known SSC markers, PDPN and PDGFRA. Notably, human P-SSCs, but not bone marrow SSCs (BM-SSCs), selectively expressed newly identified markers, LRP1 and CD13. Single-cell analysis of mouse periosteum further supported the preferential expression of LRP1 and CD13 in Prx1 P-SSCs. These LRP1CD13 human P-SSCs were perivascular cells with high osteochondrogenic but minimal adipogenic potential. In addition, LRP1CD13 human P-SSCs are maintained in vitro and self-renew in vivo upon transplantation into bone injuries in mice. When Lrp1 was conditionally deleted in Prx1-lineage cells, it led to severe bone deformity, short statue, and periosteal defects. By contrast, local treatment with a LRP1 agonist at the injury sites induced early P-SSC proliferation and bone healing. Thus, human periosteum contains unique osteochondrogenic stem cell subsets, and these P-SSCs express specific markers, LRP1 and CD13, with regulatory mechanism through LRP1 that enhances P-SSC function and bone repair.

2024-11-04 | GSE278165 | GEO

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