Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [primary chondrocytes]

ABSTRACT: Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [primary chondrocytes]

PROVIDER: PRJNA1198875 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31732245_1.fastq.gz	Fastqsanger.gz
	SRR31732245_2.fastq.gz	Fastqsanger.gz
	SRR31732246_1.fastq.gz	Fastqsanger.gz
	SRR31732246_2.fastq.gz	Fastqsanger.gz
	SRR31732247_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [primary chondrocytes]

Project description:Osteoarthritis (OA) is the most common degenerative joint disease. During its initiation and early progression a disruption in subchondral bone (SCB) remodeling, induced by excessive and cumulative mechanical loading, occurs before cartilage degeneration. While it is known that osteocytes in the SCB are mainly responsible for mechanosensing, their role in the early phases of OA are still unclear. Here, we found that mechanical stress induces SCB osteocytes to secrete extracellular vesicles (EVs) that accelerate cartilage metabolic dysregulation. By gain- and loss-of function experiments we show that such EVs via miR-23b-3p promote cartilage catabolism while inhibiting their anabolism. Mechanistically, miR-23b-3p inhibits mitophagy by targeting OTUD4 to promote this metabolic skewing. Further, by inhibiting miR-23b-3p in either osteocytes or chondrocytes we could alleviate cartilage degeneration and OA progression in a mouse model. Together, our findings show that SCB osteocytes communicate with chondrocytes via EVs and that targeting a key EV-derived miRNA can ameliorate OA progression.

2025-04-12 | GSE284358 | GEO

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [only osteocyte-enriched subchondral bone]

2025-04-12 | GSE284357 | GEO

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [EVs from osteocyte-enriched subchondral bone]

2025-04-12 | GSE284359 | GEO

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [EVs from plasma]

2025-04-12 | GSE284361 | GEO

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [only osteocyte-enriched subchondral bone]

Project description:Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [only osteocyte-enriched subchondral bone]

| PRJNA1198876 | ENA

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [EVs from osteocyte-enriched subchondral bone]

Project description:Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [EVs from osteocyte-enriched subchondral bone]

| PRJNA1198879 | ENA

Adipose-derived mesenchymal stem cell extracellular vesicles downregulate inflammation in osteoarthritis chondrocytes and cartilage explants

Project description:Osteoarthritis (OA) is a joint condition associated with articular cartilage loss, low-grade synovitis and alterations in subchondral bone and periarticular tissues. In OA, the interest for mesenchymal stem cell (MSC)-EV therapeutic applications has increased. We have assessed the immunomodulary properties of adipose-derived MSCs (AD-MSCs) microvesicles (MV) and exosomes (EX) in interleukin (IL)-1β stimulated OA chondrocytes and cartilage explants and characterized them by mass spectrometry in order to uncover novel mediators in (AD-MSC)-EV immunomodulation.

2022-02-23 | PXD009077 | Pride

Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [EVs from plasma]

Project description:Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression [EVs from plasma]

| PRJNA1198886 | ENA

Therapeutic restoration of mitochondria–endoplasmic reticulum crosstalk for osteoarthritis

Project description:Osteoarthritis is a prevalent joint disease in the aging population. The hallmark of osteoarthritis is the degeneration of the joint cartilage, characterized by changes in chondrocytes including mitochondrial dysfunction. However, the precise mechanisms of how this affects chondrocyte homeostasis and whether such processes can be explored as therapeutic targets for osteoarthritis remain unclear. Here, we show that impaired mitochondrial function and disrupted cartilage matrix metabolism due to loss of mitofusin-2 (MFN2) expression in chondrocytes leads to the development of osteoarthritis. Sirtuin-3 (SIRT3), a key regulator of mitochondrial function, plays a critical role in modulating MFN2 to restore mitochondrial dynamics, reduce fragmentation, and preserve mitochondrial function in chondrocytes. Specifically, SIRT3 directly deacetylates and indirectly deubiquitinates MFN2, preventing its degradation. MFN2-mediated mitochondrial–endoplasmic reticulum (ER) junctions support cellular homeostasis, alleviate ER stress, and maintain mitochondrial calcium ion balance, which collectively mitigate chondrocyte senescence. Extracellular vesicles engineered with MFN2 mRNA effectively prevented cartilage degeneration and restored mobility in osteoarthritic mice. These findings suggest that targeting MFN2 is a promising strategy to prevent cartilage degeneration and alleviate progression of osteoarthritis.

2025-08-31 | GSE305514 | GEO

Tiki2 maintains articular cartilage homeostasis and protects against osteoarthritis by inhibiting Wnt/β-catenin signaling

Project description:Osteoarthritis (OA) is a serious degenerative joint disease with high morbidity and is currently incurable because of its poorly defined underlying molecular basis. Here, we demonstrated that Tiki2, a membrane-tethered proteolytic Wnt inhibitor, is highly expressed in the articular chondrocytes of hyaline cartilage and that its expression negatively correlates with osteoarthritis. Tiki2 haploinsufficiency in mice causes spontaneous articular cartilage degeneration. Tiki2 deletion in chondrocytes accelerates instability-induced knee joint osteoarthritis progression in mice. Mechanistically, Tiki2 antagonizes Wnt signaling in chondrocytes and maintains chondrocyte anabolic gene expression. Moreover, intra-articular administration of a TIKI2-expressing adeno-associated virus significantly alleviated OA progression in mice, and expressing TIKI2 promoted chondrogenesis and chondrocyte redifferentiation and inhibited hypertrophic differentiation in vitro. Our results reveal the function of Tiki2 in articular cartilage homeostasis and osteoarthritis and suggest that Tiki2 is a potential target for osteoarthritis therapy.

2025-07-20 | GSE302635 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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