Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Osteocytes regulate transcortical blood vessel network by transferring mitochondria to endothelial cells in cortical bone

ABSTRACT: Osteocytes regulate transcortical blood vessel network by transferring mitochondria to endothelial cells in cortical bone

PROVIDER: PRJNA932471 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Osteocytes regulate transcortical blood vessel network by transferring mitochondria to endothelial cells in cortical bone

Project description:In this study, mitochondria were proved to be capable of delivering mitochondria to endothelial cells of transcortical blood vessel and promotes its angiogenesis. By utilizing RNA seq, we investigated the effect of osteocytes-derived mitochondria on endothelial cells.

2025-02-08 | GSE224786 | GEO

Effect of osteocytes mitochondria on chondrocytes

Project description:Effect of osteocytes mitochondria on chondrocytes

| PRJNA909166 | ENA

Effect of osteocytes mitochondria on OA chondrocytes

Project description:Effect of osteocytes mitochondria on OA chondrocytes

| PRJNA907788 | ENA

The effects of mitochondrial damages under stress or during aging on osteocytes networks homeostasis

Project description:Using oligomycin A-treated MLO-Y4 cells and primary murine aging osteocytes as a model of cells with mitochondrial dysfunction, it is demonstrated that when mitochondria are damaged, osteocytes tend to release signaling compounds including adenosine diphosphate. We identified that the nucleotide membrane receptors P2Y2 and P2Y6 transduced the ADP signal to Mfn2, a critical regulator of osteocyte mitochondrial transfer. Whole RNA sequencing (RNA-seq) analysis of mouse cortical bone showed that mitochondrial metabolism is impaired in aged osteocytes, and there are more extracellular nucleotides released into the matrix in cortical bone in aged mice as compared to that in young mice. Aging decreases expression levels of P2Y2/P2Y6 and Mfn2.

2024-01-24 | GSE235103 | GEO

Osteocytes regulate skeletal senescence during development

Project description:To understand the mechanism underlying the bone phenotype in osteocytes ablation mice.

2022-11-21 | GSE202356 | GEO

Effect of osteocytes mitochondria on chondrocytes

Project description:To investigate the regulatory role of MLO-Y4 mitochondria on chondrocytes, we isolated mitochondria from MLO-Y4 and transplanted to chondrocytes. We then performed gene expression profiling analysis using data obtained from RNA-seq of chondrocytes from vehicle group and mitochondria transplanted group.

2024-12-31 | GSE220168 | GEO

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/Î²-catenin pathway, is also essential for bone health. As osteocytes are known as the major mechanosensory cells embedded in mineralized bone matrix, osteocyte ERÎ± deletion mice (ERÎ±ÎOcy/ÎOcy) were generated by mating ERÎ± floxed mice with Dmp1-Cre mice to determine functions of ERÎ± in osteocytes. Trabecular bone mineral density of female, but not male ERÎ±ÎOcy/ÎOcy mice was significantly decreased. Bone formation parameters in ERÎ±ÎOcy/ÎOcy were significantly decreased while osteoclast parameters were unchanged. This suggests that ERÎ± in osteocytes exerts osteoprotective function by positively controlling bone formation. To identify potential targets of ERÎ±, gene array analysis of Dmp1-GFP osteocytes FACS sorted from ERÎ±ÎOcy/ÎOcy 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 Î²-catenin. Hindlimb unloading exacerbated the trabecular bone loss, but surprisingly cortical bone was resistant. These studies show that ERÎ± 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. Wild type and osteocyte-specific Estrogen Receptor alpha knock-out mice were generated. The number of both genotypes of mice was three. Calvarial osteocytes of both genotypes harboring Dmp1-GFP were extracted by sequential enzymatic digestion, followed by FACS Aria sorting and total RNAs were purified for Affymetix GeneChip microarray analysis without pooling.

2013-12-12 | E-GEOD-41997 | biostudies-arrayexpress

Effect of osteocytes mitochondria on OA chondrocytes

Project description:To investigate the regulatory role of MLO-Y4 mitochondria on OA chondrocytes, we isolated mitochondria from MLO-Y4 and transplanted to chondrocytes treated with IL-1β. We then performed gene expression profiling analysis using data obtained from RNA-seq of chondrocytes from vehicle group and mitochondria transplanted group.

2024-12-01 | GSE219238 | GEO

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

Osteocytes regulate skeletal senescence during development

Project description:Osteocytes regulate skeletal senescence during development

| PRJNA835705 | ENA