Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Decreased chondrocyte features of articular cartilage during short-term repeated overloading: a synovium-cartilage interaction via inhibin subunit beta A

ABSTRACT: The primary goal of this study is to investigate the ultrashort-term responses and molecular mechanisms in both the synovium and cartilage under conditions of excessive mechanical loading, a major contributing factor in the pathogenesis of osteoarthritis (OA). While cartilage degeneration is a hallmark of OA, the involvement of the synovium in disease progression and pain, particularly in relation to synovitis, has been increasingly recognized. Despite this, the immediate molecular changes in both tissues following mechanical stress, and the interactions between them, remain unclear. To address these gaps, we developed a mouse model that simulates excessive mechanical loading through treadmill exercise combined with weight attachment. We investigated the ultrashort-term gene expression changes in the synovium and cartilage at 1, 4, and 24 hours post-exercise using RNA sequencing (RNA-seq). Additionally, we examined the effects of repeated overloading by analyzing tissue samples from mice subjected to four consecutive days of overloading. This approach allowed us to capture both the acute and repeated stress responses in these tissues. Through transcriptomic analysis, we aimed to identify key molecular mediators driving both the rapid transcriptional changes in each tissue and the synovium-cartilage interaction.

ORGANISM(S): Mus musculus

PROVIDER: GSE280656 | GEO | 2025/03/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Rapgef3 modulates macrophage reprogramming and exacerbates synovitis and osteoarthritis under excessive mechanical loading

Project description:Evidences indicate that mechanical loading plays an important role in osteoarthritis (OA) progression, while the specific pathological changes of the synovium under excessive mechanical loading are unclear. Results showed excessive mechanical loading caused pro-inflammatory of synovial macrophages, which has been confirmed to exists in OA. High Rapgef3 expression level was found in RNA sequencing of RAW246.7 subjected to 0.5Hz-20%-cyclic tensile strain. We verified this in the synovium of OA patients and DMM-OA mice. Interestingly, the Rapgef3 content of chondrocytes was very low. Primary chondrocytes treated with Rapgef3 alone did not show metabolic phenotype, but an OA phenotype appeared when treated with Rapgef3-stimulated macrophage culture supernatant. Mechanically, excessive mechanical loading activated p65-NF-κB pathway through Rapgef3, which promoted the inflammatory of macrophage, resulting in severe articular cartilage injury. Intra-articular Rapgef3 knockout reversed synovitis and cartilage degeneration, which might provide a therapeutic target for osteoarthritis.

2024-11-04 | GSE280230 | GEO

MiR-335-5p escaped from circKIAA0586 adsorption contributes to mechanical overloading-induced cartilage degeneration by targeting HELLS (circRNA-Seq)

Project description:Mechanical overload is essential to cartilage degeneration during osteoarthritis (OA) development. Recent studies have confirmed that circular RNAs (circRNAs) are mechanically sensitive and that the circRNA-associated competitive endogenous RNA (ceRNA) network regulates cartilage degeneration and OA development. However, the involvement of the circRNA-associated ceRNA network in chondrocyte senescence induced by mechanical overloading remains unestablished.Here,we examined the circRNA, miRNA and mRNA expression of chondrocytes subjected to mechanical overloading.

2024-11-01 | GSE274761 | GEO

MiR-335-5p escaped from circKIAA0586 adsorption contributes to mechanical overloading-induced cartilage degeneration by targeting HELLS (miRNA-Seq)

2024-11-01 | GSE274760 | GEO

MiR-335-5p escaped from circKIAA0586 adsorption contributes to mechanical overloading-induced cartilage degeneration by targeting HELLS (RNA-Seq)

2024-11-01 | GSE274759 | GEO

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 [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]

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

NG2/CSPG4 regulates cartilage degeneration during TMJ osteoarthritis

Project description:Changes in the mechanical homeostasis of the temporomandibular joint (TMJ) can lead to the initiation and progression of degenerative arthropathies such as osteoarthritis (OA). Cells sense and engage with their mechanical microenvironment through interactions with the extracellular matrix. In the mandibular condylar cartilage, the pericellular microenvironment is composed of type VI collagen. NG2/CSPG4 is a transmembrane proteoglycan that binds with type VI collagen, and has been implicated in the cell stress response through mechanical loading-sensitive signaling networks including ERK 1/2. The objective of this study is to define the role of NG2/CSPG4 in the initiation and progression of TMJ OA and to determine if NG2/CSPG4 engages ERK 1/2 in a mechanical loading dependent manner. In vivo, we induced TMJ OA in control and NG2/CSPG4 knockout mice using a surgical destabilization approach. In control mice, NG2/CSPG4 is depleted during the early stages of TMJ OA and NG2/CSPG4 knockout mice have more severe cartilage degeneration, elevated expression of key OA proteases, and suppression of OA matrix synthesis genes. In vitro, we characterized the transcriptome and protein from control and NG2/CSPG4 knockout cells and found significant dysregulation of the ERK 1/2 signaling axis. To characterize the mechanobiological response of NG2/CSPG4, we applied mechanical loads on cell-agarose-collagen scaffolds using a compression bioreactor and illustrate that NG2/CSPG4 knockout cells fail to mechanically activate ERK 1/2 and are associated with changes in the expression of the same key OA biomarkers measured in vivo. Together, these findings implicate NG2/CSPG4 in the mechanical homeostasis of TMJ cartilage and in the progression of degenerative arthropathies including OA.

2022-09-24 | GSE214077 | GEO

Project description:Aging is a major risk factors for osteoarthritis (OA), and cartilage of the elder are more sensitive to mechanical loading stress. Recently, cartilage progenitor cells (CPCs) arose much interests due to its important role in maintaining cartilage homeostasis. However, the potential mechanism of increased sensitivity to mechanical stress in CPCs has not been elucidated. The aim of this study was to investigate the potential links between aging and age-related OA through establish CPCs replicative senescence model and fluid flow shear stress (FFSS) stimulated degeneration model. Small RNA and mRNA sequence were conducted to investigate miRNA-related mechanisms in this process. By gain-and-lost strategy we investigated the age-related miRNAs and their impacts on exacerbating the progression of biomechanical stimulated TMJ-OA. miR-708-5p was identified as age-related miRNA in CPCs, and TLR4 was identified as its direct target through luciferase report assay. Age-related miR-708-5p deficiency increased sensitivity of CPCs for exposure to FFSS by liberating TLR4 expression. Intra-articular delivery agomiR-708-5p alleviated TMJ osteoarthritic cartilage lesions in mice. In conclusion, age-related miR-708-5p deficiency increases the sensitivity to mechanical loading stress and promotes CPCs senescence like degeneration via TLR4.

2023-07-11 | GSE236978 | 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