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首页> 外文期刊>Life sciences >Involvement of protein kinase Cdelta in iron chelator-induced IL-8 production in human intestinal epithelial cells.
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Involvement of protein kinase Cdelta in iron chelator-induced IL-8 production in human intestinal epithelial cells.

机译：蛋白激酶Cdelta参与铁螯合剂诱导的人肠上皮细胞中IL-8的产生。

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摘要

We have shown that the bacterial iron chelator, deferoxamine (DFO), triggers inflammatory signals, including the production of CXC chemokine IL-8, in human intestinal epithelial cells (IECs) by activating ERK1/2 and p38 kinase pathways. In the present study, we show that PKCdelta, one of the novel protein kinase C (PKC) isoforms, involves in signal transduction pathways leading to DFO-induced IL-8 production. Pretreatment of human intestinal epithelial HT-29 cells with rottlerin showed remarkable inhibition of DFO-induced IL-8 production. In contrast, other PKC inhibitors such as Go6976, Go6983, GF109203X, and staurosporine revealed less or no inhibitory effects on DFO-induced IL-8 production, suggesting a potential role of PKCdelta. Accordingly, DFO caused phosphorylation of PKCdelta in the Thr505 and Ser643 residues in HT-29 cells. Transfection of dominant-negative PKCdelta vector inhibited DFO-induced PKCdelta phosphorylation as well as IL-8 promoter activity. In addition, suppression of endogenous PKCdelta by siRNA significantly reduced DFO-induced IL-8 production. Collectively, these results suggest that PKCdelta plays a pivotal role in signaling pathways leading to iron chelator-induced IL-8 production in human IECs.
机译：我们已经表明，细菌铁螯合剂去铁胺（DFO）通过激活ERK1 / 2和p38激酶途径在人肠上皮细胞（IEC）中触发炎症信号，包括CXC趋化因子IL-8的产生。在本研究中，我们显示PKCdelta，一种新型的蛋白激酶C（PKC）亚型，参与导致DFO诱导的IL-8产生的信号转导途径。用rottlerin预处理人肠上皮HT-29细胞显示出显着抑制DFO诱导的IL-8产生。相反，其他PKC抑制剂（例如Go6976，Go6983，GF109203X和星形孢菌素）显示出对DFO诱导的IL-8产生的抑制作用较小或没有抑制作用，表明PKCdelta具有潜在作用。因此，DFO导致HT-29细胞中Thr505和Ser643残基的PKCdelta磷酸化。显性阴性PKCdelta载体的转染抑制DFO诱导的PKCdelta磷酸化以及IL-8启动子活性。另外，通过siRNA抑制内源性PKCdelta可以显着降低DFO诱导的IL-8产生。总的来说，这些结果表明PKCdelta在信号通路中起关键作用，导致人IEC中铁螯合剂诱导的IL-8产生。

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