Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

β-catenin inhibits adipogenic differentiation of hypertrophic chondrocytes and promote osteogenesis

ABSTRACT: It has been shown that hypertrophic chondrocyte (HC) can become osteoblast, contributing to the formation of trabecular bone and endosteum. However, it is unclear what genes regulate the process of differentiation from chondrocyte to osteoblast. Conditional knock-out of β‑catenin in HCs can reduce the trabecular bone amount and there is also some evidence that ablation of β‑catenin in HCs can promote bone marrow adipogenesis. Conditional stabilization of β‑catenin in HCs results in osteopetrosis. In order to investigate the gene regulatory network with different dosage of β‑catenin in HC descendants (i.e. in Loss-of-Function mutant, Gain-of-Function mutant and Wildtype control), we collected HC descendant cells from proximal tibia of mice at postnatal day 5 and performed bulk RNA seq to profile the gene expression pattern in HC descendants.

ORGANISM(S): Mus musculus

PROVIDER: GSE146111 | GEO | 2020/07/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Hypertrophic chondrocytes and osteogenesis in P6 mouse tibia

Project description:It has been shown that hypertrophic chondrocyte (HC) can become osteoblast, contributing to the formation of trabecular bone and endosteum. However, it is unclear what genes regulate the process of differentiation from chondrocyte to osteoblast. Conditional knock-out of Irx 3 and Irx5 in HCs can reduce the trabecular bone amount and there is also some evidence that ablation of Irx3 and Irx5 in HCs can promote bone marrow adipogenesis. In order to investigate the gene regulatory network with different dosage of Irx3/5 in HC descendants (i.e. in Loss-of-Function mutant and heterozygous control), we collected HC descendant cells from proximal tibia of mice at postnatal day 6 and performed single cell RNA seq with 10X Genomics System to profile the gene expression pattern in HC descendants.

2023-03-13 | GSE159544 | GEO

Effect of osteoblast-specific constitutive activation of beta-catenin or deletion of FoxO1 on gene expression in mice

Project description:The gene expression of mice with osteoblast-specific beta-catenin activation or FoxO1 deactivation are each compared to that of Wt. A. Wt mice (n=4) B. Osteoblast specific beta-catenin constitutively expressed mice (n=3) C. Osteoblast specific FoxO1 deleted mice (n=3)

2014-01-21 | E-GEOD-43242 | biostudies-arrayexpress

Mouse primary osteoblasts treated with/without BMP2

Project description:Bone morphogenetic proteins (BMPs) regulate many aspects of skeletal development, including osteoblast and chondrocyte differentiation, cartilage and bone formation, and cranial and limb development. Among them, BMP2, one of the most potent osteogenic signaling molecules, stimulates osteoblast differentiation. We used cDNA microarrays to elucidate regulators of BMP-2-induced osteoblast differentiation.

2012-03-29 | E-GEOD-36925 | biostudies-arrayexpress

Collagen10-Cre;Rosa26-tdTomato e16.5 single cell RNA-sequencing

Project description:In order to assess the descendants of hypertrophic chondrocytes, we utilized Collagen10-Cre;Rosa26-tdTomato mouse total bone isolated at e16.5 by Collagenase II digestion after mechanical digestion and soft tissue removal. After sequencing and downstream analysis using Seurat, we observed clusters of cells with gene profiles matching classically defined chondrocytes, skeletal stem and progenitor cells (SSPCs), and osteoblasts. Trajectory analysis reveals that the SSPCs lie intermediate to the transition of chondrocyte to osteoblast. We conclude that hypertrophic chondrocytes dedifferentiate to this progenitor stage before further differentiation.

2022-02-16 | GSE190616 | GEO

Mouse C2C12 cells treated with/without hBMP2

Project description:Bone morphogenetic proteins (BMPs) regulate many aspects of skeletal development, including osteoblast and chondrocyte differentiation, cartilage and bone formation, and cranial and limb development. Among them, BMP2, one of the most potent osteogenic signaling molecules, stimulates osteoblast differentiation, while it inhibits myogenic differentiation in C2C12 cells. We used cDNA microarrays to elucidate regulators of BMP-2-induced osteoblast differentiation.

2011-11-11 | E-GEOD-33567 | biostudies-arrayexpress

Expression data from Dmp1-GFP sorted osteocytes

Project description:Estrogens are well known steroid hormones necessary to maintain bone health. In addition, mechanical loading, which estrogen signaling may intersect with the Wnt/β-catenin pathway, is also essential for bone health. As osteocytes are known as the major mechanosensory cells embedded in mineralized bone matrix, osteocyte ERα deletion mice (ERαΔOcy/ΔOcy) were generated by mating ERα floxed mice with Dmp1-Cre mice to determine functions of ERα in osteocytes. Trabecular bone mineral density of female, but not male ERαΔOcy/ΔOcy mice was significantly decreased. Bone formation parameters in ERαΔOcy/ΔOcy were significantly decreased while osteoclast parameters were unchanged. This suggests that ERα in osteocytes exerts osteoprotective function by positively controlling bone formation. To identify potential targets of ERα, gene array analysis of Dmp1-GFP osteocytes FACS sorted from ERαΔOcy/ΔOcy and control mice was performed. Expression of Mdk and Sostdc1, both known inhibitors of Wnt, were significantly increased without alteration of the mature osteocyte marker Sost or β-catenin. Hindlimb unloading exacerbated the trabecular bone loss, but surprisingly cortical bone was resistant. These studies show that ERα in osteocytes has osteoprotective effects in trabecular bone through regulating expression of Wnt antagonists, but conversely plays a negative role in cortical bone loss due to unloading.

2013-12-12 | GSE41997 | GEO

Comprehensive analysis on the signaling pathway of Norrie disease protein (Ndp)

Project description:Mutations in the gene for Norrie disease protein (Ndp) cause syndromic deafness and blindness. We show that cochlear function in an Ndp knockout (KO) mouse deteriorated with age: at P3-P4, hair cells (HCs) showed progressive loss of Pou4f3 and Gfi1, key transcription factors for HC maturation, and Myo7a, a specialized myosin required for normal function of HC stereocilia. Loss of expression of these genes correlated to increasing HC loss and profound hearing loss by 2 months of age. We show that overexpression of the Ndp gene in neonatal supporting cells or, remarkably, upregulation of canonical Wnt signaling in HCs rescued HCs and cochlear function. We conclude that Ndp secreted from supporting cells orchestrates a transcription factor network for the maintenance and survival of HCs and that increasing the level of b-catenin, the intracellular effector of Wnt signaling, is sufficient to replace the functional requirement for Ndp in the cochlea.

2021-09-04 | GSE173393 | GEO

Mouse primary osteoblasts treated with/without BMP2

2012-03-30 | GSE36925 | GEO

Mouse C2C12 cells treated with/without hBMP2

Project description:Bone morphogenetic proteins (BMPs) regulate many aspects of skeletal development, including osteoblast and chondrocyte differentiation, cartilage and bone formation, and cranial and limb development. Among them, BMP2, one of the most potent osteogenic signaling molecules, stimulates osteoblast differentiation, while it inhibits myogenic differentiation in C2C12 cells.

2011-11-11 | GSE33567 | GEO

PRDM proteins control Wnt/β-catenin activity to regulate craniofacial chondrocyte differentiation

Project description:Cranial neural crest (NCC)-derived chondrocyte precursors undergo a dynamic differentiation and maturation process to establish a scaffold for subsequent bone formation, alterations in which contribute to congenital birth defects. Here, we demonstrate that transcription factor and histone methyltransferase proteins Prdm3 and Prdm16 control the differentiation switch of cranial NCCs to craniofacial cartilage. Loss of either results in hypoplastic and unorganized chondrocytes due to impaired cellular orientation and polarity. We show that PRDMs regulate cartilage differentiation by controlling the timing of Wnt/β-catenin activity in strikingly different ways: prdm3 represses while prdm16 activates global gene expression, though both by regulating Wnt enhanceosome activity and chromatin accessibility. Finally, we show that manipulating Wnt/β-catenin signaling pharmacologically or generating prdm3-/-;prdm16-/- double mutants rescues craniofacial cartilage defects. Our findings reveal upstream regulatory roles for Prdm3 and Prdm16 in cranial NCCs to control Wnt/β-catenin transcriptional activity during chondrocyte differentiation to ensure proper development of the craniofacial skeleton.

2022-02-08 | GSE175767 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data