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cAMP is not involved in interleukin-1-induced interleukin-6 release from human astrocytoma cells.

作者信息

Cadman E D, Naugles D D, Lee C M

机构信息

Pharmaceutical Products Division, Abbott Laboratories, Abbott Park, IL 60064.

出版信息

Neurosci Lett. 1994 Sep 12;178(2):251-4. doi: 10.1016/0304-3940(94)90771-4.

DOI:10.1016/0304-3940(94)90771-4
PMID:7529912
Abstract

We have previously shown that activation of the phosphatidyl-inositol/phospholipase C pathway could induce interleukin 6 (IL-6) release from U373MG human astrocytomes cells. We also found that, although interleukin 1 beta (IL-1 beta) did not activate phosphatidy-linositol 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.

摘要

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