Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA474389 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7275250_1.fastq.gz | Fastqsanger.gz | |||
| SRR7275250_2.fastq.gz | Fastqsanger.gz | |||
| SRR7275251_1.fastq.gz | Fastqsanger.gz | |||
| SRR7275251_2.fastq.gz | Fastqsanger.gz | |||
| SRR7275252_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Transcriptional landscape of facet joint osteoarthritis insights into facet cartilage degeneration ( miRNA )
| PRJNA474395 | ENA
Project description:Osteoarthritis (OA) of spine (facet joints; FJ) is one of the major causes of severe low back pain and disability worldwide. The degeneration of facet cartilage is a hallmark of FJ OA. However, endogenous mechanisms that initiate degeneration of facet cartilage are unknown and there are no disease-modifying therapies to stop FJ OA. In this study we performed microRNA array analysis to identify differentially expressed microRNAs in facet cartilage from patients with FJ OA compared to facet cartilage from patients with lumbar disc herniation (LDH).
2016-03-15 | GSE79258 | GEO
Project description:microRNA expression in facet cartilage degeneration
| PRJNA315290 | ENA
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
Project description:HPIP controls osteoarthritis cartilage degeneration [ChIP-seq]
| PRJNA391302 | ENA
Project description:HPIP controls osteoarthritis cartilage degeneration [RNA-seq]
| PRJNA391184 | ENA
Project description:Osteoarthritis (OA) is a degenerative joint disease that involves destruction of articular cartilage and eventually leads to disability. Mesenchymal stem cells (MSCs) reside in healthy and diseased cartilage, and through their chondrogenic potential may provide a strategy for cartilage repair. To this end, we performed an image-based, high throughput screen and identified the small molecule, kartogenin, that promotes selective MSC differentiation into chondrocytes (EC50=100nM), shows chondroprotective effects in vitro, and is efficacious in two OA animal models. Kartogenin binds filamin A and induces chondrogenesis by regulating the CBFbeta-RUNX1 transcriptional program. This work provides new insights into the control of chondrogenesis that may ultimately lead to an effective stem-cell based therapy for osteoarthritis. one compound, three doses, two time points, a vehicle control
2012-05-01 | E-GEOD-35546 | biostudies-arrayexpress
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
Project description:Osteoarthritis is characterized by degeneration of cartilage and bone in the synovial joints. Recent findings suggest that inflammation may play a role in osteoarthritis, with synovitis being associated with the clinical symptoms of osteoarthritis. Furthermore, we have found that levels of inflammatory complement components are abnormally high in the synovial fluid of individuals with osteoarthritis. To determine whether synovial membranes could be a source of complement and other inflammatory molecules in osteoarthritic joints, we characterized the expression of genes in synovial membranes from patients with early-stage or end-stage osteoarthritis. Samples of synovial membrane were obtained from the suprapatellar pouch of patients with osteoarthritis who were treated at the Hospital for Special Surgery. Specifically, samples were from 10 patients with early-stage knee osteoarthritis who were undergoing arthroscopic procedures for degenerative meniscal tears (with documented cartilage degeneration but no full-thickness cartilage loss, Kellgren Lawrence score </=2), and from 9 patients with end-stage knee osteoarthritis ( diffuse full thickness cartilage erosion) who were undergoing total knee joint replacement. Raw data from microarray analysis of healthy synovial membranes, which were run on the same platform and array as our osteoarthritic samples, were downloaded from the NCBI Gene Expression Omnibus (accession number GSE12021) and used for comparison. The 19 new Samples of this Series were analyzed (RMA) together with 7 previously submitted healthy individual Samples (GSM175810, GSM175812, GSM176290, GSM176291, GSM176292, GSM176268, GSM176269). The complete RMA data are provided as a supplementary file on the Series record. The GSE12021 reanalyzed data are also provided as a supplementary file on the Series record. GSE32317_12genes.txt includes data from figure 1 of the paper.
2011-11-01 | E-GEOD-32317 | biostudies-arrayexpress
Project description:Osteoarthritis (OA) is a degenerative joint disease with a substantial health economic burden. There is no current treatment; instead, disease management targets the main symptoms (pain and stiffness) and culminates in joint replacement surgery. OA is a disease of cartilage degeneration, but the molecular changes leading to the development of OA are still poorly understood. In this study we compare methylation, gene transcription and protein abundance at the genome-wide level in individually-matched samples of chondrocytes extracted from affected and relatively healthy articular cartilage across 12 OA patients undergoing total knee replacement. Integration analysis highlights genes that are consistently affected at multiple levels, including AQP1, CLEC3B and COL1A1, and also relevant biological pathways such as extracellular matrix organization, collagen catabolism and proteolysis. Collectively these results provide a first view of the comprehensive molecular landscape underpinning OA development and point to potential therapeutic avenues.
2018-10-24 | PXD002014 | Pride