cAMP/PKA enhances interleukin-1β-induced interleukin-6 synthesis through STAT3 in glial cells
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- 作者：Kumiko Tanabea ; kumiko-t@m2.gyao.ne.jp" class="auth_mail" title="E-mail the corresponding author ; Osamu Kozawab ; okozawa@gifu-u.ac.jp" class="auth_mail" title="E-mail the corresponding author ; Hiroki Iidaa ; iida@gifu-u.ac.jp" class="auth_mail" title="E-mail the corresponding author
- 关键词：8-bromo cAMP ; adenosine-3&prime ; 5&prime ; -cyclic monophosphate ; 8-bromo- ; sodium salt ; CMI ; 4-cyano-3-methylisoquinoline ; CNS ; central nervous system ; DMEM ; Dulbecco's modified Eagle's medium ; EPAC ; exchange proteins directly activated by cAMP ; ELISA ; enzyme-linked immunosorbent assay ; GAPDH ; glyceraldehyde-3-phosphate dehydrogenase ; IL ; interleukin ; JAK ; Janus family of tyrosine kinase ; MAP ; mitogen-activated protein ; PGE ; prostaglandin ; PKA ; protein kinase A ; SAPK/JNK ; stress-activated protein
- 刊名：Cellular Signalling
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：28
- 期：1
- 页码：19-24
- 全文大小：686 K
文摘
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We investigated the cAMP mechanism on IL-1β-induced IL-6 synthesis amplification.
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cAMP enhanced phosphorylation of STAT3, but not IκB, p38 MAP kinase or SAPK/JNK.
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Forskolin significantly strengthened IL-1β-induced STAT3 phosphorylation.
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JAK inhibitor I suppressed the amplification by 8-bromo cAMP of IL-6 release.
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PKA inhibitor attenuated the enhancing effect of cAMP on STAT3 phosphorylation.
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