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Genome-wide DNA methylation study of hip and knee osteoarthritic and healthy cartilage reveals embryonic organ and skeletal system morphogenesis as major pathways involved in osteoarthritis

ABSTRACT: Cartilage samples were collected from hip or knee joint replacement patients either due to primary OA or hip fractures as controls. DNA was extracted from the collected cartilage and assayed by Illumina Infinium HumanMethylation450 ‎BeadChip array, which allows for the analysis of >480,000 CpG sites.

ORGANISM(S): Homo sapiens

PROVIDER: GSE73626 | GEO | 2016/07/01

SECONDARY ACCESSION(S): PRJNA297447

REPOSITORIES: GEO

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Genome-wide DNA methylation study of hip and knee osteoarthritic and healthy cartilage reveals embryonic organ and skeletal system morphogenesis as major pathways involved in osteoarthritis

Project description:Cartilage samples were collected from hip or knee joint replacement patients either due to primary OA or hip fractures as controls. DNA was extracted from the collected cartilage and assayed by Illumina Infinium HumanMethylation450 âBeadChip array, which allows for the analysis of >480,000 CpG sites. Bisulphite converted DNA from 5 hip osteoarthritic, 6 knee osteoarthritic and 7 hip healhty cartilage samples were hybridised to the Illumina Infinium HumanMethylation450 âBeadChip array

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Project description:The pathogenesis of necrosis of femoral head (NFH) remains elusive now. Limited studies were conducted to investigate the molecular mechanism of hip articular cartilage damage of NFH. We conducted a genome-wide gene expression profiling of hip articular cartilage with NFH. Hip articular cartilage specimens were collected from 12 NFH patients and 12 healthy controls. Gene expression profiling of NFH articular cartilage was carried out by Agilent Human 4x44K Gene Expression Microarray chip. Differently expressed genes were identified using the Significance Analysis of Microarrays (SAM) software.

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Osteoarthritis-related changes in gene expression in knee articular chondrocytes in a rat model of osteoarthritis.

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Project description:Aims：To establish a novel model of mechanical loading-induced knee osteoarthritis (KOA) and explore its regulatory mechanisms through transcriptomics. Methods：Knee joints of Sprague-Dawley (SD) rats were mechanically loaded with 13 N, 20 N and 27 N for 2 or 4 weeks to construct mechanically-induced KOA model. Immunohistochemistry (IHC), quantitative real-time polymerase chain reaction (qRT-PCR), Western blot, Safranin O/fast green staining, enzyme-linked immunosorbent assay (ELISA), micro-computed tomography (Micro-CT) and behavioral analysis were used to evaluate damage on the right knee joint. Transcriptomic analysis combined with validation experiments were performed to explore the regulatory mechanism of excessive mechanical loading on KOA development. Results：A vertical load of 27 N resulted in calf fractures, whereas a 13 N load did not cause remarkable pathological alteration in the knee joint. Notably, applying compression at a load of 20 N for 4 weeks (w) significantly promoted the levels of pro-inflammatory factors IL-6, IL-β and TNF-α in serum and joint fluids and markedly minimized the levels of anti-inflammatory factors IL-10 and TGF-β. Immunohistochemistry, qRT-PCR and Western blot analyses suggested that the 20 N load reduced the expression of anabolism markers (ACAN and COL2A1) and escalated the expression of catabolism markers (MMP13 and ADAMTS4). KEGG analysis and validation results showed that the PIEZ1 channel, Ca2+ signaling pathway, PI3K-AKT signaling pathway and NF-κB signaling pathway were significantly activated in the 20N-4 w group. Conclusion：Continuous loading with 20 N for 4 weeks can induce significant OA-like damage to the cartilage of the right knee in rats, which might be induced through the piezo1-Ca2+/PI3K-AKT/ NF-κB signaling pathway.

2024-09-05 | GSE276365 | GEO

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