作者: Takemasa Takii , Atsushi Ito , Kikuo Onozaki , Takayuki Matsumura
DOI:
关键词: Molecular biology 、 Endocrinology 、 Amyloid 、 Receptor expression 、 Dexamethasone 、 Cell 、 Glucocorticoid 、 Internal medicine 、 Interleukin 6 、 In vivo 、 Biology 、 Kinase
摘要: IL-1 signal is transduced through type I receptor (IL-1RI). We have recently reported that LPS augments IL-1RI mRNA expression in the hepatocytes of mice vivo, and augmentation mediated by interaction IL-1, IL-6, glucocorticoid (GC). In this study, we examined whether level reflects those cell surface molecule signaling. When primary cultured murine were treated with dexamethasone (Dex) or these two reagents synergistically up-regulated cells. 125I-labeled binding experiment showed was also treatment Dex IL-6. Scatchard analysis revealed number IL-1R increased. The increased completely inhibited an Ab against IL-1RI, indicating IL-6 augmented molecule. pretreated activation IL-1R-associated kinase response to signaling augmented. addition, following administration combination into markedly serum amyloid A. These results indicate GC augment hepatocytes, as well activation, up-regulation level, which represents a novel regulatory network between GC,