Research ExplorerPublicationsJNK1 is not essential for TNF-mediated joint disease

JNK1 is not essential for TNF-mediated joint disease

Standard

JNK1 is not essential for TNF-mediated joint disease. / Köller, Marcus; Hayer, Silvia; Redlich, Kurt; Ricci, Romeo; David, Jean-Pierre; Steiner, Günter; Smolen, Josef S; Wagner, Erwin F; Schett, Georg.

In: ARTHRITIS RES THER, Vol. 7, No. 1, 01.01.2005, p. R166-73.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Köller, M, Hayer, S, Redlich, K, Ricci, R, David, J-P, Steiner, G, Smolen, JS, Wagner, EF & Schett, G 2005, 'JNK1 is not essential for TNF-mediated joint disease', ARTHRITIS RES THER, vol. 7, no. 1, pp. R166-73. https://doi.org/10.1186/ar1473

APA

Köller, M., Hayer, S., Redlich, K., Ricci, R., David, J-P., Steiner, G., Smolen, J. S., Wagner, E. F., & Schett, G. (2005). JNK1 is not essential for TNF-mediated joint disease. ARTHRITIS RES THER, 7(1), R166-73. https://doi.org/10.1186/ar1473

Vancouver

Köller M, Hayer S, Redlich K, Ricci R, David J-P, Steiner G et al. JNK1 is not essential for TNF-mediated joint disease. ARTHRITIS RES THER. 2005 Jan 1;7(1):R166-73. https://doi.org/10.1186/ar1473

Bibtex

@article{8c28616b2d984c0ab3589024d9bb18ef,
title = "JNK1 is not essential for TNF-mediated joint disease",
abstract = "Tumour necrosis factor (TNF) signalling molecules are considered as promising therapeutic targets of antirheumatic therapy. Among them, mitogen-activated protein kinases are thought to be of central importance. Herein, we investigate the role in vivo of TNF-alpha signalling through c-Jun N-terminal kinase (JNK)1 in destructive arthritis. Human TNF transgenic (hTNFtg) mice, which develop inflammatory arthritis, were intercrossed with JNK1-deficient (JNK1-/-) mice. Animals (n = 35) of all four genotypes (wild-type, JNK1-/-, hTNFtg, JNK1-/-hTNFtg) were assessed for clinical and histological signs of arthritis. Clinical features of arthritis (swelling and decreased grip strength) developed equally in hTNFtg and JNK1-/-hTNFtg mice. Histological analyses revealed no differences in the quantity of synovial inflammation and bone erosions or in the cellular composition of the synovial infiltrate. Bone destruction and osteoclast formation were observed to a similar degree in hTNFtg and JNK1-/-hTNFtg animals. Moreover, cartilage damage, as indicated by proteoglycan loss in the articular cartilage, was comparable in the two strains. Intact phosphorylation of JNK and c-Jun as well as expression of JNK2 in the synovial tissue of JNK1-/-hTNFtg mice suggests that signalling through JNK2 may compensate for the deficiency in JNK1. Thus, JNK1 activation does not seem to be essential for TNF-mediated arthritis.",
keywords = "Animals, Arthritis, Experimental, Bone and Bones, Cartilage, Articular, Crosses, Genetic, Genotype, Humans, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Mitogen-Activated Protein Kinase 8, Mitogen-Activated Protein Kinase 9, Osteoclasts, Phosphorylation, Protein Processing, Post-Translational, Proteoglycans, Proto-Oncogene Proteins c-jun, Recombinant Fusion Proteins, Signal Transduction, Single-Blind Method, Synovial Membrane, Tumor Necrosis Factor-alpha",
author = "Marcus K{\"o}ller and Silvia Hayer and Kurt Redlich and Romeo Ricci and Jean-Pierre David and G{\"u}nter Steiner and Smolen, {Josef S} and Wagner, {Erwin F} and Georg Schett",
year = "2005",
month = jan,
day = "1",
doi = "10.1186/ar1473",
language = "English",
volume = "7",
pages = "R166--73",
journal = "ARTHRITIS RES THER",
issn = "1478-6354",
publisher = "Springer",
number = "1",

}

RIS

TY - JOUR

T1 - JNK1 is not essential for TNF-mediated joint disease

AU - Köller, Marcus

AU - Hayer, Silvia

AU - Redlich, Kurt

AU - Ricci, Romeo

AU - David, Jean-Pierre

AU - Steiner, Günter

AU - Smolen, Josef S

AU - Wagner, Erwin F

AU - Schett, Georg

PY - 2005/1/1

Y1 - 2005/1/1

N2 - Tumour necrosis factor (TNF) signalling molecules are considered as promising therapeutic targets of antirheumatic therapy. Among them, mitogen-activated protein kinases are thought to be of central importance. Herein, we investigate the role in vivo of TNF-alpha signalling through c-Jun N-terminal kinase (JNK)1 in destructive arthritis. Human TNF transgenic (hTNFtg) mice, which develop inflammatory arthritis, were intercrossed with JNK1-deficient (JNK1-/-) mice. Animals (n = 35) of all four genotypes (wild-type, JNK1-/-, hTNFtg, JNK1-/-hTNFtg) were assessed for clinical and histological signs of arthritis. Clinical features of arthritis (swelling and decreased grip strength) developed equally in hTNFtg and JNK1-/-hTNFtg mice. Histological analyses revealed no differences in the quantity of synovial inflammation and bone erosions or in the cellular composition of the synovial infiltrate. Bone destruction and osteoclast formation were observed to a similar degree in hTNFtg and JNK1-/-hTNFtg animals. Moreover, cartilage damage, as indicated by proteoglycan loss in the articular cartilage, was comparable in the two strains. Intact phosphorylation of JNK and c-Jun as well as expression of JNK2 in the synovial tissue of JNK1-/-hTNFtg mice suggests that signalling through JNK2 may compensate for the deficiency in JNK1. Thus, JNK1 activation does not seem to be essential for TNF-mediated arthritis.

AB - Tumour necrosis factor (TNF) signalling molecules are considered as promising therapeutic targets of antirheumatic therapy. Among them, mitogen-activated protein kinases are thought to be of central importance. Herein, we investigate the role in vivo of TNF-alpha signalling through c-Jun N-terminal kinase (JNK)1 in destructive arthritis. Human TNF transgenic (hTNFtg) mice, which develop inflammatory arthritis, were intercrossed with JNK1-deficient (JNK1-/-) mice. Animals (n = 35) of all four genotypes (wild-type, JNK1-/-, hTNFtg, JNK1-/-hTNFtg) were assessed for clinical and histological signs of arthritis. Clinical features of arthritis (swelling and decreased grip strength) developed equally in hTNFtg and JNK1-/-hTNFtg mice. Histological analyses revealed no differences in the quantity of synovial inflammation and bone erosions or in the cellular composition of the synovial infiltrate. Bone destruction and osteoclast formation were observed to a similar degree in hTNFtg and JNK1-/-hTNFtg animals. Moreover, cartilage damage, as indicated by proteoglycan loss in the articular cartilage, was comparable in the two strains. Intact phosphorylation of JNK and c-Jun as well as expression of JNK2 in the synovial tissue of JNK1-/-hTNFtg mice suggests that signalling through JNK2 may compensate for the deficiency in JNK1. Thus, JNK1 activation does not seem to be essential for TNF-mediated arthritis.

KW - Animals

KW - Arthritis, Experimental

KW - Bone and Bones

KW - Cartilage, Articular

KW - Crosses, Genetic

KW - Genotype

KW - Humans

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Mice, Transgenic

KW - Mitogen-Activated Protein Kinase 8

KW - Mitogen-Activated Protein Kinase 9

KW - Osteoclasts

KW - Phosphorylation

KW - Protein Processing, Post-Translational

KW - Proteoglycans

KW - Proto-Oncogene Proteins c-jun

KW - Recombinant Fusion Proteins

KW - Signal Transduction

KW - Single-Blind Method

KW - Synovial Membrane

KW - Tumor Necrosis Factor-alpha

U2 - 10.1186/ar1473

DO - 10.1186/ar1473

M3 - SCORING: Journal article

C2 - 15642137

VL - 7

SP - R166-73

JO - ARTHRITIS RES THER

JF - ARTHRITIS RES THER

SN - 1478-6354

IS - 1

ER -