Comparison of the Damaged Cartilage with the Non-weight Bearing Healthy Cartilage
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ABSTRACT:
PROVIDER: PRJNA530239 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The cartilage samples from patient with Internatinaol Cartilage Repair Society's Scoring 3-4 cartilage defects were analysed in order to understand the differences between healthy and damaged cartilage tissues from the knee.
2019-04-02 | GSE129147 | GEO
Project description:This experiment captures the expression of genes between two sites of human cartilage within the same patients to allow investigation of genomic responses to damage during osteoarthritis. Eight patients with symptomatic OA undergoing total knee replacement (n=8, age range 65-79 years, mean age 70.3) were used in this study. Cartilage from paired osteochondral samples were isolated from the intact PLC (posterior lateral condyle) and the damaged DMC (distal medial condyle) for RNA-seq analysis.
2016-04-06 | E-MTAB-4304 | biostudies-arrayexpress
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:Osteoclasts are multinucleated, bone-resorbing cells. However, they also digest cartilage during skeletal maintenance, development and in degradative conditions including osteoarthritis, rheumatoid arthritis and primary bone sarcoma. This study explores the mechanisms behind the osteoclast–cartilage interaction. Human osteoclasts differentiated on acellular human cartilage expressed osteoclast marker genes (e.g. CTSK, MMP9) and proteins (TRAP, VNR), visibly damaged the cartilage surface and released glycosaminoglycan in a contact-dependent manner. Direct co-culture with chondrocytes during differentiation increased large osteoclast formation (p < 0.0001) except when co-cultured on dentine, when osteoclast formation was inhibited (p = 0.0002). Osteoclasts cultured on dentine inhibited basal cartilage degradation (p = 0.012). RNA-seq identified MMP8 overexpression in osteoclasts differentiated on cartilage versus dentine (8.89-fold, p = 0.0133), while MMP9 was the most highly expressed MMP. Both MMP8 and MMP9 were produced by osteoclasts in osteosarcoma tissue. This study suggests that bone-resident osteoclasts and chondrocytes exert mutually protective effects on their ‘native’ tissue. However, when osteoclasts contact non-native cartilage they cause degradation via MMPs. Understanding the role of osteoclasts in cartilage maintenance and degradation might identify new therapeutic approaches for pathologies characterized by cartilage degeneration.
2021-12-01 | GSE166535 | GEO
Project description:Owing to the limited regenerative capacity of articular cartilage, damaged cartilage does not spontaneously heal over time. Various scientific efforts have been made to improve damaged articular cartilage. Nevertheless, no single approach has achieved a promising outcome for the damaged cartilage. Meanwhile, owing to the increasing cost of drug development, drug repositioning has been actively attempted. We aimed to identify the drug that can improve the cartilage defect, using chondrogenesis related microarray data recruited from the Gene Expression Omnibus (GEO) public database. Furthermore, we attempted to experiment using cellular and animal models to verify the cartilage regeneration potential for the identified drug. To screen for drugs that promote cartilage restoring, chondrogenesis related microarray data were collected from the GEO public database. The GSE69110, GSE107649, GSE111822, and GSE116173 datasets from the GEO were used to identify cartilage differentiation-related genes. Differentially expressed genes were identified using StringTie, and drug data were extracted from the Drug-Gene Interaction database. The effect of aripiprazole on cartilage was evaluated in aripiprazole-treated adipose-derived mesenchymal stem cells (ADMSCs) and chondrocyte using qRT-PCR and 3D pellet culture. The cartilage restoring efficacy was verified in vivo by mixing it with a scaffold and introducing it into the artificially damaged cartilage of Sprague-Dawley rats. Next, mRNA was sequenced for mechanistic analysis. As a result, aripiprazole significantly increased the mRNA expression of COL2A1 and SOX9, two cartilage differentiation-related genes, and chondrogenic condensation in vitro. Moreover, it effectively promoted cartilage regeneration in the cartilage defect rat model. Analysis of mRNA sequencing data from chondrocyte treated with aripiprazole, using KEGG and GOBP, indicated that aripiprazole significantly upregulates genes associated with ribosomes and cytoplasmic translation, thus promoting chondrogenesis. In conclusion, we discovered that aripiprazole can effectively improve damaged cartilage, providing a promising approach for cartilage regeneration.
2024-12-30 | GSE271026 | GEO
Project description:Protective effects of ginsenoside Rh2 on doxorubicin damaged hearts from breast tumor bearing mice
| PRJNA775988 | ENA
Project description:RNA-Seq analysis of human intact and damaged osteoarthrtitic cartilage following total knee replacement.
| PRJEB12436 | ENA
Project description:Anorexia is frequently observed during cancer and associated with increased morbidity and mortality. Our previous work has shown the presence of transcription factors in the hypothalamus of anorectic tumor-bearing rats. The aim of the present study was, therefore, to assess expression of neuropeptides, neurotransmitter-synthesizing enzymes and receptors in this structure. Morris hepatoma 7777 cells injected subcutaneously in Buffalo rats provoked a 15% reduction in food intake and 10% lower body weight when the tumor represented 1-2% of body mass. Real-time PCR showed that tumor-bearing rats did not display the increase in hypothalamic agouti-related peptide mRNA observed in food-restricted weight-matched animals. These findings indicate that blunted hypothalamic AgRp mRNA expression underlies cancer-associated anorexia.
2010-04-10 | GSE18688 | GEO
Project description:Successfully replacing damaged cartilage with tissue-engineered constructs requires integration with the host tissue and could benefit from leveraging the native tissue's intrinsic healing capacity; however, efforts are limited by a poor understanding of how cartilage repairs minor defects. Here, we investigated the conditions that foster natural cartilage tissue repair to identify strategies that might be exploited to enhance the integration of engineered/ grafted cartilage with host tissue. We damaged porcine articular cartilage explants and using a combination of pulsed SILAC-based proteomics, ultrastructural imaging, and catabolic enzyme blocking strategies reveal that integration of damaged cartilage surfaces is not driven by neo-matrix synthesis, but rather local depletion of proteoglycans. ADAMTS4 expression and activity are upregulated in injured cartilage explants, but integration could be reduced by inhibiting metalloproteinase activity with TIMP3. These observations suggest that catabolic enzyme-mediated proteoglycan depletion likely allows existing collagen fibrils to undergo cross-linking, fibrillogenesis, or entanglement, driving integration. Catabolic enzymes are often considered pathophysiological markers of osteoarthritis. Our findings suggest that damage-induced upregulation of metalloproteinase activity may be a part of a healing response that tips towards tissue destruction under pathological conditions and in osteoarthritis, but could also be harnessed in tissue engineering strategies to mediate repair. Statement of significance: Cartilage tissue engineering strategies require graft integration with the surrounding tissue; however, how the native tissue repairs minor injuries is poorly understood. We applied pulsed SILACbased proteomics, ultrastructural imaging, and catabolic enzyme blocking strategies to a porcine cartilage explant model and found that integration of damaged cartilage surfaces is driven by catabolic enzyme-mediated local depletion of proteoglycans. Although catabolic enzymes have been implicated in cartilage destruction in osteoarthritis, our findings suggest that damage-induced upregulation of metalloproteinase activity may be a part of a healing response that tips towards tissue destruction under pathological conditions. They also suggest that this natural cartilage tissue repair process could be harnessed in tissue engineering strategies to enhance the integration of engineered cartilage with host tissue.
2022-07-18 | PXD035246 | Pride
Project description:Analysis of basal gene expression of the protective bones of the skull (parietals) and weight-bearing bones of the limb (ulnae) Experiment Overall Design: RNA extraction from normal bone
2008-11-22 | E-GEOD-12966 | biostudies-arrayexpress