Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA992054 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25180119.fastq.gz	Fastqsanger.gz
	SRR25180119_1.fastq.gz	Fastqsanger.gz
	SRR25180119_2.fastq.gz	Fastqsanger.gz
	SRR25180120.fastq.gz	Fastqsanger.gz
	SRR25180120_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

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

Miz1 is required to maintain autophagic flux

Project description:Miz1 is required to maintain autophagic flux

| PRJNA210788 | 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

Histone methylation regulator PTIP is required to maintain normal and leukemic bone marrow niches

Project description:The bone is essential for locomotion, calcium storage and harboring the hematopoietic stem cells (HSCs) that supply the body with mature blood cells throughout life. HSCs reside at the interface of the bone and bone marrow (BM), where active bone remodeling takes place. Although the cellular components of the BM niche have been characterized, little is known about its epigenetic regulation. Here we find that the histone methylation regulator PTIP (Pax interaction with transcription-activation domain protein-1) is required to maintain the integrity of the BM niche by promoting osteoclast differentiation. PTIP directly promotes chromatin changes required for the expression of Pparg (Peroxisome proliferator-activated receptor-γ), a transcription factor essential for osteoclastogenesis. PTIP deletion leads to a drastic reduction of HSCs in the BM and induces extramedullary hematopoiesis. Furthermore, exposure of acute myeloid leukemia cells to a PTIP-deficient BM microenvironment leads to a reduction in leukemia initiating cells (LICs) and increased survival upon transplantation. Taken together, our data identify PTIP as a novel epigenetic regulator of osteoclastogenesis that is required for the integrity of the BM niche to sustain both normal hematopoiesis and leukemia.

2018-09-24 | GSE118329 | GEO

Human SMARCA5 Is Continuously Required to Maintain Nucleosome Spacing

Project description:Human SMARCA5 Is Continuously Required to Maintain Nucleosome Spacing

| PRJNA673246 | ENA

Piezo1 balances the osteogenic-tenogenic plasticity of periosteal progenitor cells through the YAP pathway

Project description:The extremity tendons and bones are derived from limb bud mesenchyme, which eventually become cells of different tissues. Despite their common origin, it was widely believed that tenocytes and skeletal cells are distinct lineages without interconversion. However, we found that periosteal skeletal progenitor cells could transform between osteogenic and tenogenic commitment. SCX can label the periosteal progenitor cell population. Loss of Piezo1 arrests the periosteal progenitor cells in a progenitor state. Piezo1 deficiency leads to upregulation of Scx expression due to the inhibited YAP nuclear localization. Loss of Piezo1 showed increased tenogenic marker genes and decreased osteogenic marker genes. The periosteal progenitor cells can regenerate the injured tendon more robustly when Piezo1 is absent. Taken together, our data reveal that periosteal SCX+ progenitor cells compromise the osteogenic ability and acquire the tenocyte-biased lineage commitment after loss of Piezo1, providing a strategy to modulate the periosteal progenitor cells for tissue regeneration.

2025-10-22 | GSE249206 | GEO

Mechanosensitive Piezo1 is crucial for periosteal stem cell-mediated fracture healing

Project description:Mechanosensitive Piezo1 is crucial for periosteal stem cell-mediated fracture healing

2024-12-19 | GSE266774 | GEO

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

Cell autonomous expression of Bcl6 is required to maintain lineage identity of mouse CCR6+ ILC3s

Project description:Cell autonomous expression of Bcl6 is required to maintain lineage identity of mouse CCR6+ ILC3s

| PRJNA913925 | ENA

Cell autonomous expression of Bcl6 is required to maintain lineage identity of mouse CCR6+ ILC3s

Project description:Cell autonomous expression of Bcl6 is required to maintain lineage identity of mouse CCR6+ ILC3s

| PRJNA909759 | ENA