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TL1A deficiency attenuates osteoarthritis by regulating oxidative stress-induced senescence in articular chondrocytes [II]

ABSTRACT: TL1A deficiency attenuates osteoarthritis by regulating oxidative stress-induced senescence in articular chondrocytes [II]

PROVIDER: PRJNA1208007 | ENA |

REPOSITORIES: ENA

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TL1A deficiency attenuates osteoarthritis by regulating oxidative stress-induced senescence in articular chondrocytes [I]

Project description:TL1A deficiency attenuates osteoarthritis by regulating oxidative stress-induced senescence in articular chondrocytes [I]

| PRJNA1208006 | ENA

TL1A deficiency attenuates osteoarthritis by regulating oxidative stress-induced senescence in articular chondrocytes [II]

Project description:Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by progressive cartilage degradation, chronic inflammation, and chondrocyte senescence. Tumor necrosis factor-like cytokine 1A (TL1A), a member of the TNF superfamily, has recently been implicated in regulating inflammatory processes and tissue remodeling. However, its precise role in OA pathogenesis remains incompletely understood. In this study, we investigated the impact of TL1A deficiency on OA progression and its underlying mechanism with a focus on oxidative stress-induced chondrocyte senescence.

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TL1A deficiency attenuates osteoarthritis by regulating oxidative stress-induced senescence in articular chondrocytes [I]

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Comparison between articular chondrocytes and mesenchymal stromal cells for the production of articular chondrocyte implants

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Rip3 effect on mouse articular chondrocytes

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Project description:Gene expression profiling of mouse articular chondrocytes infected with Ad-C or Ad-Nox4 In this study, we have attempted to explore the effects of Nox4 and have identified numerous genes which are involved in osteoarthritis pathogenesis.

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ActivinA effect on mouse articular chondrocytes

Project description:Gene expression profiling of mouse articular chondrocytes infected with Ad-C or Ad-Activin A In this study, we have attempted to explore the effects of Activin A and have identified numerous genes which are involved in osteoarthritis pathogenesis.

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Articular cartilage proteome differentiates by zones during osteoarthritis

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.

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Microarray analysis of human articular chondrocytes stimulated with Wnt3a in presence/absence of the CaMKII inhibitor KN93

Project description:The scope of the analysis was to discriminate between CaMKII-dependent and independent targets of Wnt3a stimulation in human articular chondrocytes. Chondrocytes were isolated from preserved areas of the articular cartilage removed from 4 patients affected by osteoarthritis. The samples were stimulated with KN92 (inactive analogue of the CaMKII inhibitor KN93), KN92+Wnt3a and KN93+Wnt3a.

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

Project description:Cartilage destruction in osteoarthritis (OA) results from disturbed chondrocyte metabolism. Here, we used microarrays to show that TGF alpha and CCL2 are simultaneously upregulated in a rat model of OA and cooperate to drive cartilage degradation. The goals of the experiments included here were to a) characterize gene expression in knee joint articular chondrocytes at various stages of development of OA (2 and 8 weeks after surgical induction of OA), and b) to establish trends in gene expression among groups of genes related to the TGF alpha-EGFR axis, over time, in OA. The model chosen to study these results has been previously validated (Appleton, CT et al, 2007, Arthritis Rheum) and used to describe similar gene expression results at a different time point (4 weeks) after induction of OA. The rat model of OA involves surgical destabilization of the knee joint, followed by forced low-intensity mobilization over several weeks; a sham surgery is used as the control (representing a healthy non-OA knee joint) wherein a surgical incision is made but not structural (i.e. ligamentous) modification is made to the joint. Altogether, our data indicate that TGF and CCL2 cooperate to drive cartilage degradation in osteoarthritis. A total of 12 samples were analyzed. 3 replicates were used per condition: OA surgery at 2 weeks, OA surgery at 8 weeks, Sham (control) surgery at 2 weeks and Sham surgery at 8 weeks. Expression of OA samples was assessed relaitve to Sham (control) expression levels.

2012-11-15 | E-GEOD-42295 | biostudies-arrayexpress

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