TNF inhibits insulin induced STAT5 activation in differentiated mouse muscle cells pmi28

FEBS Letters

Pfizenmaier, Klaus¹  Wernig, Anton²  Döppler, Heike¹  Storz, Peter¹  Müller, Gertraud¹ 

[1] Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, D-70569 Stuttgart, Germany;Institute of Physiology, University of Bonn, Wilhelmstr. 31, D-53111 Bonn, Germany

关键词: Insulin resistance;    Tumor necrosis factor;    Skeletal muscle;    STAT5;    AP;    alkaline phosphatase;    BSA;    bovine serum albumin;    EMSA;    electrophoretic mobility shift assay;    IRβ;    insulin receptor β chain;    IRS-1;    insulin receptor substrate-1;    JAK;    janus kinase;    NF-κB;    nuclear factor κB;    NIDDM;    non-insulin dependent diabetes mellitus;    PAGE;    polyacrylamide gel electrophoresis;    PBS;    phosphate buffered saline;    PI-3 kinase;    phosphatidylinositol-3 kinase;    PMSF;    phenylmethylsulfonyl fluoride;    PY;    phosphotyrosine;    SH;    SRC homology;    STAT;    signal transducer activator of transcription;    TNF;    tumor necrosis factor;   

DOI  :  10.1016/S0014-5793(98)01421-5

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Tumor necrosis factor (TNF) plays a central role in the state of insulin resistance leading to type II diabetes. We here describe the crosstalk of TNF with insulin signaling cascades in the mouse muscle cell line pmi28. TNF downregulated insulin induced insulin receptor kinase activity and insulin induced activation of the transcription factor STAT5. Our results provide evidence that the inhibitory crosstalk between TNF and insulin in skeletal muscle cells comprises an interference with the expression of STAT5 regulated genes which may play an important role in the manifestation and/or progression of insulin resistance in muscle cells.

【 授权许可】

Unknown