86 research outputs found
252 F-SPONDIN MEDIATES CATABOLIC EFFECTS ON ARTICULAR CHONDROCYTES VIA ITS THROMBOSPONDIN REPEAT (TSR) DOMAIN
Activation of stress-activated protein kinase in osteoarthritic cartilage: evidence for nitric oxide dependence
AbstractObjective We have demonstrated in bovine chondrocytes that nitric oxide (NO) mediates IL1 dependent apoptosis under conditions of oxidant stress. This process is accompanied by activation of c-Jun NH2-terminal kinase (JNK; also called stress-activated protein kinase). In these studies we examined activation of JNK in explant cultures of human osteoarthritic cartilage obtained at joint replacement surgery and we characterized the role of peroxynitrite to act as an upstream trigger.Design A novel technique to isolate chondrocyte proteins (<10% of total cartilage protein) from cartilage specimens was developed. It was used to analyse JNK activation by a western blot technique. To examine the hypothesis that chondrocyte JNK activation is a result of increased peroxynitrite, in vitro experiments were performed in which cultured chondrocytes were incubated with this oxidant.Results Activated JNK was detected in the cytoplasm of osteoarthritis (OA) affected chondrocytes but not in that of controls. In vitro, chondrocytes produce NO and superoxide anion. IL-1 (48h), which induces nitric oxide synthase, resulted in an activation of JNK; this effect was reversed by N-monomethylarginine (NMA). TNFα treated chondrocytes at 48h produce superoxide anion (EPR method). Exposure of cells to peroxynitrite led to an accumulation of intracellular oxidants, in association with JNK activation and cell death by apoptosis.Conclusion We suggest that JNK activation is among the IL-1 elicited responses that injure articular chondrocytes and this activation of JNK is dependent on intracellular oxidant formation (including NO peroxynitrite). In addition, the extraction technique here described is a novel method that permits the quantitation and study of proteins such as JNK involved in the signaling pathways of chondrocytes within osteoarthritic cartilage
F-spondin (spondin-1) null mice exhibit increased bone formation, decreased osteoclast function and accelerated osteoarthritis
Elevated peripheral blood leukocyte inflammatory gene expression in radiographic progressors with symptomatic knee osteoarthritis: NYU and OAI cohorts
073 MIR-7 AND MIR-130B ARE DIFFERENTIALLY REGULATED DURING MESENCHYMAL STEM CELL COMMITMENT
P180 PROSTAGLANDIN E2 INDUCES MITOCHONDRIAL DYSFUNCTION IN OSTEOARTHRITIC CHONDROCYTES AND EXERTS CATABOLIC EFFECTS VIA THE EP4 RECEPTOR
208 RESVERATROL, THE ANTIOXIDANT OF RED WINE, PREVENTS IL-1 MEDIATED MITOCHONDRIAL DYSFUNCTION AND ATP DEPLETION: ROLE OF PGE2 AS A CAUSE OF CELLULAR ENERGY DEPLETION
62 PERIOSTIN, AN OSTEOBLAST STIMULATING FACTOR, REGULATES CARTILAGE METABOLISM VIA MMP-13 ACTIVATION
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