We are analyzing https://link.springer.com/article/10.1186/ar1797.

Title:
Tumour necrosis factor activates the mitogen-activated protein kinases p38α and ERK in the synovial membrane in vivo | Arthritis Research & Therapy
Description:
Tumour necrosis factor (TNF) is considered to be a major factor in chronic synovial inflammation and is an inducer of mitogen-activated protein kinase (MAPK) signalling. In the present study we investigated the ability of TNF to activate MAPKs in the synovial membrane in vivo. We studied human TNF transgenic mice – an in vivo model of TNF-induced arthritis – to examine phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun amino terminal kinase (JNK) and p38MAPKα in the inflamed joints by means of immunoblot and immunohistochemistry. In addition, the effects of systemic blockade of TNF, IL-1 and receptor activator of nuclear factor-κB (RANK) ligand on the activation of MAPKs were assessed. In vivo, overexpression of TNF induced activation of p38MAPKα and ERK in the synovial membrane, whereas activation of JNK was less pronounced and rarely observed on immunohistochemical analysis. Activated p38MAPKα was predominantly found in synovial macrophages, whereas ERK activation was present in both synovial macrophages and fibroblasts. T and B lymphocytes did not exhibit major activation of any of the three MAPKs. Systemic blockade of TNF reduced activation of p38MAPKα and ERK, whereas inhibition of IL-1 only affected p38MAPKα and blockade of RANK ligand did not result in any decrease in MAPK activation in the synovial membrane. These data indicate that TNF preferentially activates p38MAPKα and ERK in synovial membrane exposed to TNF. This not only suggests that targeted inhibition of p38MAPKα and ERK is a feasible strategy for blocking TNF-mediated effects on joints, but it also shows that even currently available methods to block TNF effectively reduce activation of these two MAPKs.
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Keywords {🔍}

activation, synovial, erk, tnf, pmapkα, arthritis, article, mice, jnk, pubmed, kinase, google, scholar, mapk, cas, cells, protein, membrane, htnftg, factor, necrosis, macrophages, fibroblasts, rheumatoid, mitogenactivated, blockade, tissue, fig, expression, wildtype, lymphocytes, signalling, mapks, activated, vivo, effects, joint, cytokine, tumour, inflammation, kinases, study, human, rank, ligand, inflammatory, significantly, rheum, extracellular, cjun,

Topics {✒️}

c-jun n-terminal kinase c-jun amino-terminal kinase c-jun amino-terminal kinases anti-tumour necrosis factor mitogen-activated protein kinase tumour necrosis factor extracellular signal-regulated kinase il-1β-induced cox-2 expression mitogen-activated protein kinases tumor necrosis factor stress-activated protein kinases 5-bromo-4-chloro-3-indolyl phosphate ultra-turrax t50 homogenizer protein phosphatase-mediated inhibition article download pdf phosphate-buffered saline [pbs] hsf1/hsp70 stress response rabbit experimental osteoarthritis rat monoclonal antibody cell-type specific antibodies fc-osteoprotegerin fusion protein p38 protein kinases nuclear factor-κb c-kit ligand stimulation wild-type mice exhibited normal wild-type mice phosphatase inhibitor cocktail cell-specific antibody related subjects tnf promotes synovitis nf-kappab transcription factors full size image synovial fibroblast privacy choices/manage cookies fc fusion protein tnf-mediated cellular effects activator protein-1 complex article number r1140 cell-specific markers tnf-induced mapk activation tnf equally activates full access authors’ original file epidermal growth factor tnf-induced mapk induction reduces inflammatory response blocking tnf-mediated effects rat adjuvant arthritis weakly increased activation pooled protein extracts

Schema {🗺️}

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         headline:Tumour necrosis factor activates the mitogen-activated protein kinases p38α and ERK in the synovial membrane in vivo
         description:Tumour necrosis factor (TNF) is considered to be a major factor in chronic synovial inflammation and is an inducer of mitogen-activated protein kinase (MAPK) signalling. In the present study we investigated the ability of TNF to activate MAPKs in the synovial membrane in vivo. We studied human TNF transgenic mice – an in vivo model of TNF-induced arthritis – to examine phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun amino terminal kinase (JNK) and p38MAPKα in the inflamed joints by means of immunoblot and immunohistochemistry. In addition, the effects of systemic blockade of TNF, IL-1 and receptor activator of nuclear factor-κB (RANK) ligand on the activation of MAPKs were assessed. In vivo, overexpression of TNF induced activation of p38MAPKα and ERK in the synovial membrane, whereas activation of JNK was less pronounced and rarely observed on immunohistochemical analysis. Activated p38MAPKα was predominantly found in synovial macrophages, whereas ERK activation was present in both synovial macrophages and fibroblasts. T and B lymphocytes did not exhibit major activation of any of the three MAPKs. Systemic blockade of TNF reduced activation of p38MAPKα and ERK, whereas inhibition of IL-1 only affected p38MAPKα and blockade of RANK ligand did not result in any decrease in MAPK activation in the synovial membrane. These data indicate that TNF preferentially activates p38MAPKα and ERK in synovial membrane exposed to TNF. This not only suggests that targeted inhibition of p38MAPKα and ERK is a feasible strategy for blocking TNF-mediated effects on joints, but it also shows that even currently available methods to block TNF effectively reduce activation of these two MAPKs.
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      headline:Tumour necrosis factor activates the mitogen-activated protein kinases p38α and ERK in the synovial membrane in vivo
      description:Tumour necrosis factor (TNF) is considered to be a major factor in chronic synovial inflammation and is an inducer of mitogen-activated protein kinase (MAPK) signalling. In the present study we investigated the ability of TNF to activate MAPKs in the synovial membrane in vivo. We studied human TNF transgenic mice – an in vivo model of TNF-induced arthritis – to examine phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun amino terminal kinase (JNK) and p38MAPKα in the inflamed joints by means of immunoblot and immunohistochemistry. In addition, the effects of systemic blockade of TNF, IL-1 and receptor activator of nuclear factor-κB (RANK) ligand on the activation of MAPKs were assessed. In vivo, overexpression of TNF induced activation of p38MAPKα and ERK in the synovial membrane, whereas activation of JNK was less pronounced and rarely observed on immunohistochemical analysis. Activated p38MAPKα was predominantly found in synovial macrophages, whereas ERK activation was present in both synovial macrophages and fibroblasts. T and B lymphocytes did not exhibit major activation of any of the three MAPKs. Systemic blockade of TNF reduced activation of p38MAPKα and ERK, whereas inhibition of IL-1 only affected p38MAPKα and blockade of RANK ligand did not result in any decrease in MAPK activation in the synovial membrane. These data indicate that TNF preferentially activates p38MAPKα and ERK in synovial membrane exposed to TNF. This not only suggests that targeted inhibition of p38MAPKα and ERK is a feasible strategy for blocking TNF-mediated effects on joints, but it also shows that even currently available methods to block TNF effectively reduce activation of these two MAPKs.
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         Tumour Necrosis Factor
         Synovial Membrane
         Synovial Tissue
         Synovial Fibroblast
         MAPK Activation
         Rheumatology
         Orthopedics
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