LPS and TNFα induce SOCS3 mRNA and inhibit IL‐6‐induced activation of STAT3 in macrophages

FEBS Letters

Häussinger, Dieter²  Schaper, Fred¹  Schmitt, Marcus²  Schmitz, Jochen¹  Nimmesgern, Ariane³  Frisch, Wiltrud¹  Bode, Johannes G.¹  Heinrich, Peter C.¹  Graeve, Lutz¹ 

[1] Institut für Biochemie, Klinikum der RWTH Aachen, Pauwelsstraße 30, 52057 Aachen, Germany;Klinik für Gastroenterologie, Hepatologie und Infektiologie, Medizinische Klinik der Heinrich-Heine Universität, 40255 Düsseldorf, Germany;Interdisziplinäres Zentrum für klinische Forschung, Biomat, RWTH Aachen, 52074 Aachen, Germany

关键词: Cytokine cross-talk;    Lipopolysaccharide resistance;    Inflammation;    Cytokine signaling;    DMEM;    Dulbecco's modified Eagle's medium;    EMSA;    electrophoretic mobility shift assay;    GAPDH;    glycerin aldehyde-3-phosphate dehydrogenase;    IFN;    interferon;    LPS;    lipopolysaccharide;    MAP kinase;    mitogen-activated protein kinase;    STAT;    signal transducer and activator of transcription;    SOCS;    suppressor of cytokine signaling;    TNFα;    tumor necrosis factor α;   

DOI  :  10.1016/S0014-5793(99)01662-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Recent findings indicate that cytokine signaling can be modulated by other mediators of simultaneously activated signal transduction pathways. In this study we show that LPS and TNFα are potent inhibitors of IL-6-mediated STAT3 activation in human monocyte derived macrophages, rat liver macrophages and RAW 264.7 mouse macrophages but not in human hepatoma cells (HepG2) or in rat hepatocytes. Accordingly, LPS and TNFα were found to induce the expression of SOCS3 mRNA in each of the investigated type of macrophages but not in HepG2 cells. Using a specific inhibitor, evidence is presented that the p38 MAP kinase might be involved, especially for the inhibitory effect of TNFα.

【 授权许可】

Unknown