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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Roles of ERK and NF-κB in Interleukin-8 Expression in Response to Heat Shock Protein 22 in Vascular Smooth Muscle Cells
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Roles of ERK and NF-κB in Interleukin-8 Expression in Response to Heat Shock Protein 22 in Vascular Smooth Muscle Cells

机译：ERK和NF-κB在白细胞介素8表达对血管平滑肌细胞热休克蛋白22反应中的作用。

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摘要

Heat shock proteins (HSPs) serve as molecular chaperones and play a role in cell protection from damage in response to stress stimuli. The aim of this article is to investigate whether HSP22 affects IL-8 expression in vascular smooth muscle cells (VSMCs), and which cellular factors are involved in the HSP-mediated IL-8 induction in that cell type in terms of mitogen activated protein kinase (MAPK) and transcription element. Exposure of aortic smooth muscle cells (AoSMCs) to HSP22 not only enhanced IL-8 release but also induced IL-8 transcript via promoter activation. HSP22 activated ERK and p38 MAPK in AoSMCs. HSP22-induced IL-8 release was inhibited by U0126, but not by SB202190. A mutation in the IL-8 promoter region at the binding site of NF-κB, but not AP-1 or C/EBP, impaired promoter activation in response to HSP22. Delivery of IκB, but not dominant negative c-Jun, lowered HSP22-induced IL-8 release from AoSMCs. These results suggest that HSP22 induces IL-8 in VSMCs via ERK1/2, and that transcription factor NF-kB may be required for the HSP22-induced IL-8 up-regulation.
机译：热激蛋白（HSP）充当分子伴侣，并在细胞保护中免受应激刺激的损害中发挥作用。本文的目的是研究HSP22是否影响血管平滑肌细胞（VSMC）中IL-8的表达，以及哪种细胞因子以促分裂原活化蛋白激酶的形式参与了HSP介导的IL-8诱导（MAPK）和转录元件。将主动脉平滑肌细胞（AoSMCs）暴露于HSP22不仅增强了IL-8的释放，而且还通过启动子激活诱导了IL-8的转录。 HSP22激活了AoSMC中的ERK和p38 MAPK。 HSP22诱导的IL-8释放受U0126抑制，但不受SB202190抑制。 IL-8启动子区域中的NF-κB结合位点处的突变，而不是AP-1或C / EBP处的突变，削弱了响应HSP22的启动子激活。 IκB的传递，但不是显性阴性c-Jun的传递，降低了HSP22诱导的AoSMCs IL-8释放。这些结果表明，HSP22通过ERK1 / 2诱导VSMC中的IL-8，并且HSP22诱导的IL-8上调可能需要转录因子NF-kB。

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