CAMP IS NOT INVOLVED IN INTERLEUKIN-1-INDUCED INTERLEUKIN-6 RELEASE FROM HUMAN ASTROCYTOMA-CELLS

被引:11
作者
CADMAN, ED
NAUGLES, DD
LEE, CM
机构
[1] Neuroscience Research, Pharmaceutical Products Division, Abbott Laboratories, Abbott Park
关键词
INTERLEUKIN; 1; GLIA; ADENYLATE CYCLASE; FORSKOLIN; ISOPROTERENOL; DIBUTYRYL CAMP; 3-ISOBUTYL-1-METHYLXANTHINE;
D O I
10.1016/0304-3940(94)90771-4
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We have previously shown that activation of the phosphatidyl-inositol/phospholipase C pathway could induce interleukin 6 (IL-6) release from U373MG human astrocytoma cells. We also found that, although interleukin 1 beta (IL-1 beta) did not activate phosphatidylinositol turnover, it induced a robust release of IL-6. In the present study, we examined the role of adenylate cyclase/cyclic 3',5'-adenosine monophosphate (cAMP) pathway in IL-6 release. Agents,which mimicked (dibutyryl cAMP) or stimulated (isoproterenol and forskolin) cAMP formation were found to induce IL-6 release and their effects could be potentiated by 3-isobutyl-1-methylxanthine (IBMX), a phosphodiesterase inhibitor. On the other hand, in spite of its robust action on IL-6 release, IL-1 beta did not stimulate cAMP formation. Other possible signal transduction mechanisms involved in IL-1 beta-induced IL-6 release are discussed.
引用
收藏
页码:251 / 254
页数:4
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