Interleukin 1 activates jun N‐terminal kinases JNK1 and JNK2 but not extracellular regulated MAP kinase (ERK) in human glomerular mesangial cells

FEBS Letters

von der Ohe, Juliane¹  Kracht, Michael¹  Szamel, Martha¹  Resch, Klaus¹  Saklatvala, Jeremy²  Uciechowski, Peter¹ 

[1] Institute for Molecular Pharmacology, Medical School Hannover, D-30625 Hannover, Germany;Cytokine Laboratory, Babraham Institute, Babraham, Cambridge CB2 4AT, UK

关键词: Interleukin;    Jun N-terminal kinase;    Human mesangial cell;    IL-1;    interleukin 1;    TNF;    tumor necrosis factor;    JNK;    jun N-terminal kinase;    SAPK;    stress-activated protein kinase;    PMA;    phorbol 12-myristate 13-acetate;    bFGF;    basic fibroblast growth factor;    PDGF;    platelet-derived growth factor;    GM-CSF;    granulocyte-macrophage colony-stimulating factor;    M-CSF;    macrophage colony-stimulating factor;    LPS;    lipopolysaccharide;    TGF-β;    transforming growth factor β;   

DOI  :  10.1016/0014-5793(96)00967-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Interleukin 1 (IL-1) potently activates human glomerular mesangial cells (HMC). In cytosolic extracts of IL-1-stimulated HMC or in anion exchange chromatography fractions we could not find any change in phosphorylation of myelin basic protein (MBP), a good substrate for extracellular regulated kinase (ERK). In contrast, IL-1 stimulated GST-jun kinase activity at least 10-fold. The jun kinase activity could be characterised as JNK1 and JNK2 at the protein and mRNA level. IL-1, TNF, UV light and osmotic stress, but not PMA, LPS, IL-3, IL-4, IL-6, IL-8, IL-10, IL-13, GM-CSF, PDGF, bFGF, TGF-β and interferon-γ were able to stimulate jun kinase activity in HMC, suggesting that jun kinase is selectively mediating signal transduction of the proinflammatory cytokines IL-1 and TNF as well as of cellular stress in HMC.

【 授权许可】

Unknown