Transcriptome comparison of cartilage from patients with and without osteoarthritis
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PROVIDER: PRJNA483972 | ENA |
REPOSITORIES: ENA
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Project description:Objective: To assess the impact of osteoarthritis (OA) on the transcripts and biological process in the articular cartilage between patients with and without OA. Design: Patients undergoing arthroscopic partial meniscectomy (APM) without any evidence for OA and patients undergoing total knee arthroplasty (TKA) due to end-stage OA were consented. Healthy-appearing cartilage was garnered from the non-weight bearing site of the medial intercondylar notch. RNA preparation was subjected to SurePrint G3 human 8X60K RNA microarrays to probe differentially expressed (DE) transcripts followed by computational exploration of underlying biological processes and pathways. Real-time PCR was performed on selected transcripts to validate microarrays data. Results: We identified 603 transcripts significantly (FDR <0.05) differentially expressed (293 elevated, 310 repressed) between APM and TKA samples (1.5 fold). Among these, CFD, CSN1S1, TSPAN11, CSF1R and CD14 were the most prominent transcripts elevated in TKA group, CHI3L2, MEG3, HILPDA, COL3A1, COL27A and FGF2 were most highly repressed in TKA samples. Few long intergenic non-coding RNAs (linRNAs), and small nuclear RNAs (snoRNAs) were also differentially expressed between the two groups. Conclusions: Numerous transcripts with potential relevance to the pathogenesis of OA are DE in OA and non-OA cartilage. These data suggest an involvement of metabolic signaling and epigenetic markers (lincRNAs, snoRNAs) in cartilage.
2018-08-02 | GSE117999 | GEO
Project description:Osteoarthritis causes pain and functional disability for over 500 million people worldwide and characterized by progressive loss of cartilage from the articulating surfaces of diarthrodial joints. Although the etiology of the disease is unknown, it is widely accepted that these degenerative changes arise from an imbalance of synthetic and degradative pathways that control cartilage extracellular matrix metabolism. Genome-wide U133A Affymetrix oligonucleotide array set was used to comprehensively investigate the expression pattern in non-osteoarthritis (normal) and cartilage obtained from OA patients undergoing knee replacement surgery. This study was undertaken to better understand the molecular basis of the disease and to provide relevant insight into phenotypical alterations and mechanisms involved in OA pathogenesis.
2021-03-18 | GSE169077 | GEO
Project description:Osteoarthritis (OA) is the most prevalent joint disease with the typifying feature being the progressive degradation of articular cartilage during disease progression. In this study we used whole transcriptome RNA-seq as a tool to compare gene expression changes between age-matched osteoarthritic human hip OA cartilage (n=10) compared to control (neck of femur fracture) cartilage (n=6) [GSE107308]. All cartilage was from patients undergoing acetabulofemoral joint replacement. Cartilage RNA was isolated from cartilage within 2 hr of joint replacement surgery, mRNA was polyA purified and transcript expression was analysed using 78-base paired-end sequencing generating on average 28 million reads/sample sequencing. The data shows excellent correlation with our previous microarray data but identifies significantly more differentially expressed transcripts plus novel transcript variants, several of which have been validated by real-time qPCR. Our work sheds further light on chondrocyte transcriptome expression and highlights gene expression changes and novel transcripts potentially important in osteoarthritis progression
2019-03-01 | GSE111357 | 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:HPIP controls osteoarthritis cartilage degeneration
| PRJNA391300 | ENA
Project description:Articular cartilage is deprived of blood vessels and nerves, and the only cells residing in this tissue are chondrocytes. The molecular properties of the articular cartilage and the architecture of the extracellular matrix demonstrate a complex structure that differentiates on the depth of tissue. Osteoarthritis (OA) is a degenerative joint disease, the most common form of arthritis, affecting the whole joint. It is associated with ageing and affects the joints that have been continually stressed throughout life including the knees, hips, fingers, and lower spine region. OA is a multifactorial condition of joint characterised by articular cartilage loss, subchondral bone sclerosis, and inflammation leading to progressive joint degradation, structural alterations, loss of mobility and pain. Articular cartilage biology is well studied with a focus on musculoskeletal diseases and cartilage development. However, there are relatively few studies focusing on zonal changes in the cartilage during osteoarthritis.
2022-05-19 | PXD029116 | Pride
Project description:Cartilage mineralization is a tightly controlled process, imperative for skeletal growth and fracture repair. However, in osteoarthritis (OA), cartilage mineralization may impact the joint range of motion, inflict pain and may increase chances for joint effusion. Here we attempt to understand the link between inflammation and cartilage mineralization by targeting SIRT1 and LEF1, both reported to have contrasting effects on cartilage.
2022-05-16 | GSE200522 | GEO
Project description:RNA-sequencing analysis of hand cartilage tissue from osteoarthritis patients with/without common polymorphic variants in ALDH1A2 gene
| PRJNA895460 | ENA
Project description:The regeneration of diseased hyaline cartilage remains a great challenge, mainly because degeneration activities after major injury or due to age-related processes overwhelm the self-renewal capacity of the tissue. We show that repair tissue from human articular cartilage of late stages of osteoarthritis harbor a unique progenitor cell population, termed chondrogenic progenitor cells exhibiting stem cell characteristics, such as multipotency, lack of immune system activation and, in particular, migratory activity. The isolated CPC exhibit a high chondrogenic potential and were able to populate diseased tissue in vivo. Moreover, down-regulation of the osteogenic transcription factor runx-2 enhanced the expression of the chondrogenic transcription factor sox-9 and consequently the matrix synthesis potential of chondrogenic progenitor cells. Our results, while offering new insight into the biology of progenitor cells from diseased cartilage tissue, might assist future strategies to treat late stages of osteoarthritis. Experiment Overall Design: Characterization chondrogenic progenitor cells in P1 of 3 male and 3 female patients with late-stage OA in comparison to healthy chondrocytes in P1
2008-04-07 | E-GEOD-10575 | biostudies-arrayexpress
Project description:Osteoarthritis is characterized by cartilage destruction, chronic inflammation, and subchondral sclerosis. Evidence showed that nuclear receptor family is closely associated with cartilage damage in an unclear molecular mechanism. Here, we investigated the role and molecular mechanism of the retinoic acid receptor-related orphan receptor-α (RORα), an important member of nuclear receptor, in regulating cartilage degradation and osteoarthritis pathogenesis. Investigation to osteoarthritis clinical specimen showed that the degree of RORα elevation is positively correlated with the severity of osteoarthritis and cartilage damage. In an in vivo osteoarthritis models induced by anterior crucial ligament transaction, intraarticularly injection of siRora adenovirus reversed the cartilage damage. RORα knock-down increased the protein expression level of anabolic factor such as type II collagen, Aggrecan, and decreased the expression of catabolic factor. RNA-seq data suggested IL-6/STAT3 pathway is significantly down-regulated. Mechanistically, RORα knock-down decreased the expression level of both IL-6 and phosphorylated STAT3. RORα exerted its effect on IL-6/STAT3 signaling in two different ways, which includes interaction with STAT3 and IL6 promoter. Taken together, our findings indicated the pivotal role of RORα/IL-6/STAT3 axis in osteoarthritis progression and confirmed RORα knock-down exerted therapeutic effect in human chondrocyte thus providing a potential drug target in osteoarthritis therapy.
2021-04-20 | GSE172291 | GEO