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Homo sapiens

ABSTRACT: HPIP controls osteoarthritis cartilage degeneration [ChIP-seq]

PROVIDER: PRJNA391302 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5725510_1.fastq.gz	Fastqsanger.gz
	SRR5725510_2.fastq.gz	Fastqsanger.gz
	SRR5725511_1.fastq.gz	Fastqsanger.gz
	SRR5725511_2.fastq.gz	Fastqsanger.gz
	SRR5725512_1.fastq.gz	Fastqsanger.gz

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Project description:HPIP controls osteoarthritis cartilage degeneration [RNA-seq]

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Project description:The purpose of this study was to identify potential serum microRNA (miRNA) biomarkers of cartilage degeneration comparing preclinical mouse models of post-traumatic osteoarthritis and inflammatory arthritis.

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microRNA expression in facet cartilage degeneration

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).

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Gene expression in synovial membranes from patients with early and end-stage osteoarthritis

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

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

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

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Project description:Osteoarthritis (OA) is an aging-related degenerative joint disease without effective therapeutic. In the early stage of OA, mild synovitis has been proven to induce normal cartilage lesions. However, the mechanism is poorly defined. Here, we identified that the extracellular vesicles (EVs) derived from synovial inflammatory macrophages regulate the autophagy function of chondrocytes, acting as the dominant inducer of the onset of cartilage degeneration in normal and OA joints. Mechanistically, the active transfer of miR-155-5p via EVs from synovial inflammatory macrophages to chondrocytes accelerates cartilage degeneration by suppressing GSK 3β/mTORC1 axis-mediated autophagy function during OA progression.

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