TNF-alpha induces interleukin-8 and endothelin-1 expression in human endothelial cells with different redox pathways.

TNF-alpha induces interleukin-8 and endothelin-1 expression in human endothelial cells with different redox pathways.
复制标题

TNF-α 通过不同的氧化还原途径诱导人内皮细胞中白细胞介素 8 和内皮素 1 的表达。

DOI:
10.1016/j.bbrc.2004.12.109
复制
发表时间:
2005
期刊:
Biochemical and biophysical research communications.
影响因子:
--
通讯作者:
Chen,Changyi
Chen,Changyi
中科院分区:
--
文献类型:
--
作者:
Zhao,Ruo-Zhi;Chen,Xilin;Yao,Qizhi;Chen,Changyi

文献摘要

被引文献

相似文献

我们研究了TNF-α对白细胞介素-8 (IL-8)和内皮素-1 (ET-1)表达的影响及其不同的信号转导途径。用TNF-α处理人真皮微血管内皮细胞(HMECs)。Northern blot分析,TNF-α浓度为50、100、200和400U/ml时,与对照组相比,IL-8 mRNA的表达分别显著增加206%、252%、211%和158% (p<0.05)。通过腺病毒介导的基因转移或添加外源过氧化氢(H2O2)过表达人超氧化物歧化酶(SOD)可显著增强TNF-α-诱导的IL-8 mRNA表达。50、100和200U/ml TNF-α处理HMECs后,ET-1 mRNA表达量分别显著增加71%、82%和66% (p<0.05)。SOD基因转移和外源h2o2可显著抑制TNF-α-诱导的ET-1 mRNA表达。因此,TNF-α可能通过不同的氧化还原信号通路显著诱导hmec中IL-8和ET-1基因的表达。h2o2增强TNF-α-诱导的IL-8表达,抑制TNF-α-诱导的ET-1表达。
We investigated the effect of TNF-α on interleukin-8 (IL-8) and endothelin-1 (ET-1) expression, and their different signal transduction pathways. Human dermal microvascular endothelial cells (HMECs) were treated with TNF-α. By Northern blot analysis, TNF-α at 50, 100, 200, and 400U/ml significantly induced IL-8 mRNA expression by 206%, 252%, 211%, and 158%, respectively, as compared to controls (p<0.05). Overexpression of human superoxide dismutase (SOD) by adenovirus-mediated gene transfer or addition of exogenous hydrogen peroxide (H2O2) significantly enhanced TNF-α-induced IL-8 mRNA expression. Furthermore, HMECs treated with TNF-α at 50, 100, and 200U/ml significantly increased ET-1 mRNA expression by 71%, 82%, and 66%, respectively (p<0.05). By contrast, SOD gene transfer and exogenous H2O2significantly inhibited TNF-α-induced ET-1 mRNA expression. Thus, TNF-α significantly induces both IL-8 and ET-1 gene expression in HMECs possibly through different redox signaling pathways. H2O2enhances TNF-α-induced IL-8 expression, but inhibits TNF-α-induced ET-1 expression.