Cytokine-Hormone Interactions: Tumor Necrosis Factor α Impairs Biologic Activity and Downstream Activation Signals of the Insulin-Like Growth Factor I Receptor in Myoblasts

TNFα is elevated following damage to skeletal muscle. Here we provide evidence that TNFα acts on muscle cells to induce a state of IGF-I receptor resistance. We establish that TNFα inhibits IGF-I-stimulated protein synthesis in primary porcine myoblasts. Similar results were observed in C2C12 murine...

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Veröffentlicht in:	Endocrinology (Philadelphia) 2003-07, Vol.144 (7), p.2988-2996
Hauptverfasser:	Broussard, Suzanne R, MCCusker, Robert H, Novakofski, Jan E, Strle, Klemen, Hong Shen, Wen, Johnson, Rodney W, Freund, Gregory G, Dantzer, Robert, Kelley, Keith W
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antineoplastic Agents - pharmacology Biological and medical sciences Cell activation Cell Death - drug effects Fundamental and applied biological sciences. Psychology Growth factors Insulin Insulin Receptor Substrate Proteins Insulin-like growth factor I Insulin-like growth factors Intracellular Signaling Peptides and Proteins Life Sciences Muscles Myoblasts Myoblasts, Skeletal - cytology Myoblasts, Skeletal - drug effects Myoblasts, Skeletal - metabolism Myogenin Myogenin - biosynthesis Phosphoproteins - metabolism Phosphorylation Phosphorylation - drug effects Protein Biosynthesis Protein folding Protein synthesis Proteins Receptor, IGF Type 1 - metabolism Receptors Signal Transduction - drug effects Skeletal muscle Swine Tumor Necrosis Factor-alpha - pharmacology Tumor necrosis factor-α Tyrosine Tyrosine - metabolism
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