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Senescent tissue-resident mesenchymal stromal cell is an internal source of inflammation in human osteoarthritic cartilage

ABSTRACT: Senescent tissue-resident mesenchymal stromal cell is an internal source of inflammation in human osteoarthritic cartilage

PROVIDER: PRJNA735255 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14736904_1.fastq.gz	Fastqsanger.gz
	SRR14736904_2.fastq.gz	Fastqsanger.gz
	SRR14736905_1.fastq.gz	Fastqsanger.gz
	SRR14736905_2.fastq.gz	Fastqsanger.gz
	SRR14736906_1.fastq.gz	Fastqsanger.gz

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Senescent tissue-resident mesenchymal stromal cell is an internal source of inflammation in human osteoarthritic cartilage

Project description:RNAseq analysis indicates that the transition from normal cartilage stromal cells (nCSC) to OA-MSC during aging results in activation of SASP gene expression.

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Senescent Tissue-Resident Mesenchymal Stromal Cells Are an Internal Source of Inflammation in Human Osteoarthritic Cartilage.

Project description:Human osteoarthritic cartilage contains not only chondrocytes (OACs), but also mesenchymal stromal cells (OA-MSCs), whose abundance increases during osteoarthritis (OA). However, it is not clear how OA-MSC contributes to OA pathogenesis. Here, we show that aging OA-MSC plays an important role in cell senescence, fibrosis, and inflammation in cartilage. Protein array analysis indicates that OA-MSC expresses pro-inflammatory senescence associated secretory phenotype (SASP) including IL-1β, IL-6, IL-8, and CXCL1, 5, and 6, which play key roles in OA pathogenesis. OAC is a main recipient of the inflammatory signals by expressing receptors of cytokines. RNAseq analysis indicates that the transition from normal cartilage stromal cells (NCSCs) to OA-MSC during aging results in activation of SASP gene expression. This cell transition process can be recapitulated by a serial passage of primary OAC in cell culture comprising (1) OAC dedifferentiation into NCSC-like cells, and (2) its subsequent senescence into pro-inflammatory OA-MSC. While OAC dedifferentiation is mediated by transcriptional repression of chondrogenic gene expression, OA-MSC senescence is mediated by transcriptional activation of SASP gene expression. We postulate that, through replication-driven OAC dedifferentiation and mesenchymal stromal cell (MSC) senescence, OA-MSC becomes an internal source of sterile inflammation in human cartilage joint.

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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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Expression data of osteoarthritic and healthy human labrum cells

Project description:Osteoarthritic cartilage has largely been investigated, however supporting structures as the acetabular labrum are less investigated. In this studies we aimed to identify differences in gene expression between healthy and osteoarthritic labrum cells we used the microarray as a discovery tool to identify possible new targets in hip osteoarthritis pathology

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Project description:Aging is a major risk factors for osteoarthritis (OA), and cartilage of the elder are more sensitive to mechanical loading stress. Recently, cartilage progenitor cells (CPCs) arose much interests due to its important role in maintaining cartilage homeostasis. However, the potential mechanism of increased sensitivity to mechanical stress in CPCs has not been elucidated. The aim of this study was to investigate the potential links between aging and age-related OA through establish CPCs replicative senescence model and fluid flow shear stress (FFSS) stimulated degeneration model. Small RNA and mRNA sequence were conducted to investigate miRNA-related mechanisms in this process. By gain-and-lost strategy we investigated the age-related miRNAs and their impacts on exacerbating the progression of biomechanical stimulated TMJ-OA. miR-708-5p was identified as age-related miRNA in CPCs, and TLR4 was identified as its direct target through luciferase report assay. Age-related miR-708-5p deficiency increased sensitivity of CPCs for exposure to FFSS by liberating TLR4 expression. Intra-articular delivery agomiR-708-5p alleviated TMJ osteoarthritic cartilage lesions in mice. In conclusion, age-related miR-708-5p deficiency increases the sensitivity to mechanical loading stress and promotes CPCs senescence like degeneration via TLR4.

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