Protein kinase C-dependent pathway is critical for the production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6)
Protein kinase C-dependent pathway is critical for the production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6)
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DOI：
10.1006/cyto.1998.0496
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发表时间：
1999-11-01
期刊：
影响因子：
3.8
通讯作者：
Maslinski, W
中科院分区：
文献类型：
--
作者：
Kontny, E;Ziólkowska, M;Maslinski, W
作者假设某些 PKC 亚型在诱导促炎细胞因子（TNF-α、IL-1β、IL-6）合成中发挥重要作用。为了检验这一假设，将选定的 PKC 亚型的胞质到膜的易位与体外培养的人单核细胞中测试的细胞因子产生相关联。据报道，在用佛波酯（PMA）处理的单核细胞中，PKC亚型α、βII、δ和ε的易位先于细胞因子合成。此外，Calphostin C 存在时发生的 PKC 易位的特异性抑制反映在下游事件中：缺乏 MAP 激酶磷酸化、AP-1 转录因子丧失 DNA 结合能力以及促炎细胞因子合成减少。因此，PKC 同工型 α、β II、δ 和 ε 发生胞质到膜的易位，随后激活： (1) MAP 激酶； (2) AP-1转录因子，可能代表诱导信号级联导致人单核细胞中TNF-α、IL-1β、IL-6合成的关键步骤。 (C) 1999 年学术出版社。
The authors hypothesized that certain PKC isoforms play an important role in the induction of pro-inflammatory cytokine (TNF-alpha, IL-1 beta, IL-6) synthesis. To test this hypothesis, the cytosol-to-membrane translocation of select PKC isoforms with tested cytokine production in human monocytes cultured in vitro was correlated. It is reported that in monocytes treated with phorbol ester (PMA), translocation of PKC isoforms alpha, beta II, delta and epsilon precede cytokine synthesis. Moreover, specific inhibition of PKC translocation that occurs in the presence of Calphostin C is reflected in downstream events: lack of MAP kinases phosphorylation, loss of DNA binding ability by AP-1 transcription factor, and the reduction of pro-inflammatory cytokine synthesis. Thus, the cytosol-to-membrane translocation of PKC isoforms alpha, beta II, delta and epsilon with the subsequent activation of: (1) MAP kinases; and (2) AP-1 transcription factor, may represent critical steps ill the induction of signalling cascade leading to TNF-alpha, IL-1 beta, IL-6 synthesis in human monocytes. (C) 1999 Academic Press.