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

ABSTRACT: Identification of LRP1 and CD13 expressing human periosteal cells for stem cell-mediated bone repair

PROVIDER: PRJNA1157865 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30578455.fastq.gz	Fastqsanger.gz
	SRR30578456.fastq.gz	Fastqsanger.gz
	SRR30578457.fastq.gz	Fastqsanger.gz

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

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 | GSE276574 | GEO

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

2024-11-04 | GSE278165 | GEO

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

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

| PRJNA1165790 | ENA

YAP regulates periosteal expansion in early fracture repair.

Project description:Periosteal expansion is a key process in the early stages of bone fracture repair. The periosteum is typically quiescent, but upon fracture it expands, periosteal cells proliferate and contribute to the formation of a cartilaginous callus . The early expansion of the periosteum is tightly regulated at the transcriptional level. However, the molecular mechanisms behind periosteal expansion are unknown. Here, we show that Yes-Associated Protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) mediate periosteal expansion and periosteal cell proliferation. Bone fracture results in increased numbers of YAP-expressing periosteal cells. Deletion of YAP from Osterix (Osx) expressing periosteal cells impairs early periosteal expansion. Mechanistically, YAP regulates both cell intrinsic and extrinsic transcriptional programs that allow for periosteal expansion. Specifically, we identified Bmp4 as a cell extrinsic factor regulated by YAP, that rescues the impairment of periosteal expansion upon YAP deletion. Together, these data establish YAP mediated molecular mechanisms that allow for periosteal expansion in the early stages of fracture repair.

2025-01-07 | GSE280239 | GEO

YAP regulates periosteal expansion in early fracture repair.

Project description:YAP regulates periosteal expansion in early fracture repair.

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RNA expression profiling of CD13/CD33-positive and CD13/CD33-negative B-ALL patients [mRNA expression]

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RNA expression profiling of CD13/CD33-positive and CD13/CD33-negative B-ALL patients [miRNA expression]

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Transcriptomic analysis of primary CD105+CD90+CD13- and CD105+CD90+CD13+ mesenchymal cells in human lung

Project description:Primary mesenchymal CD105+CD90+CD13- and CD105+CD90+CD13+ populations from human lung were isolated and characterized using bulk population mRNA sequencing to understand differences between these populations.

2021-12-24 | GSE173738 | GEO

Comparison of gene expression in CD13 wild type versus Knock out Macrophages

Project description:The robust and consistent expression of the CD13 cell surface marker on very early as well as differentiated myeloid hematopoietic cells has prompted numerous investigations seeking to define roles for CD13 in myeloid cells. To directly address the function of myeloid CD13 we created a CD13 null mouse and assessed the responses of purified primary macrophages or dendritic cells from wild type and CD13 null animals in cell assays and inflammatory disease models where CD13 has been previously implicated. We find that mice lacking CD13 develop normally with normal hematopoietic profiles. Moreover, in in vitro assays, CD13 appears to be largely dispensable for the aspects of phagocytosis, proliferation and antigen presentation that we tested, but may contribute to adhesion to endothelial cells. In vivo assessment of four inflammatory disease models showed that lack of CD13 has little effect on disease onset or progression. Nominal alterations in gene expression levels between CD13 wild type and null macrophages argue against compensatory mechanisms. Analysis of the dataset with Ingenuity Pathway Analysis software did not suggest that loss of CD13 resulted in a purturbation of any specific biological pathways, processes or networks. Therefore, while CD13 is highly expressed on myeloid cells and is a reliable marker of the myeloid lineage of both normal and leukemic cells, it is not a critical regulator of hematopoietic development, hemostasis or myeloid cell function.

2010-09-30 | GSE20985 | GEO

Sfrp4 is Required to Maintain Ctsk-Lineage Periosteal Stem Cell Niche Function

Project description:The periosteum contains cells which function as a reservoir of stem cells and progenitors and contribute to cortical expansion during growth, cortical bone homeostasis and repair. However, the local or paracrine factors that govern stem cell renewal and differentiation within the periosteal niche remains elusive. Cathepsin K (Ctsk) together with additional cell surface markers marks a subset of stem cells in the periosteum (PSC) which possess self-renewal ability and inducible multipotency. These PSCs produce osteoblasts mediating periosteal bone formation and fracture repair. Sfrp4 is expressed in periosteal Ctsk-lineage cells and using CtskCre mice that are either wild type or Sfrp4-/-, we report here that Sfrp4 deletion decreases the pool of PSCs, impairs their self-renewal, their ability to give rise to their derivatives and their clonal multipotency for differentiation into osteoblasts and chondrocytes in vitro and formation of bone organoids in vivo. Bulk RNA sequencing analysis in Ctsk-lineage PSCs demonstrated that Sfrp4 deletion leads to downregulation of signaling pathways associated with skeletal development, positive regulation of bone mineralization and wound healing. Sfrp4 deletion hampers the Ctsk-lineage PSC response and recruitment after bone injury and leads to an impaired periosteal response. Periosteal Ctsk-lineage cells respond to PTH(1-34) treatment with an increase in the % of PSCs, a response not seen in the absence of Sfrp4. Importantly, bone histomorphometry analysis showed that in the absence of Sfrp4, PTH(1-34)-dependent increase in cortical thickness, periosteal bone formation is markedly impaired.

2024-08-13 | GSE236686 | GEO

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