Activation and regulation of Hsp32 and Hsp70
Activation and regulation of Hsp32 and Hsp70
复制标题
DOI：
10.1046/j.1432-1327.2000.01112.x
复制
发表时间：
2000-02-01
期刊：
影响因子：
--
通讯作者：
Stuhlmeier, KM
中科院分区：
文献类型：
--
作者：
Stuhlmeier, KM
内皮细胞（EC）在炎症反应的传播中起关键作用。更好地了解EC中的炎症过程可能会提供控制炎症的新方法。我们在这里报告，已知的抗氧化剂吡咯烷二硫代氨基甲酸酯（PDTC）导致EC中的热休克蛋白70（Hsp 70）以及Hsp 32的时间和剂量依赖性激活。我们进一步证明，PDTC激活热休克因子1（HSF 1），参与上调热休克蛋白的几个转录因子之一。更重要的是，我们证明了Hsp 32和Hsp 70可以独立于转录因子核因子κ B（NF-κ B）上调。所提供的数据提供了对Hsp 32和Hsp 70调节机制的进一步了解，以及进一步将这些基因与其他所谓的“保护性基因”区分开来，所述保护性基因的上调依赖于NF-κ B的活化。这些结果表明，Hsp 32和Hsp 70可能是理想的候选保护基因。Hsp 32和Hsp 70提供了许多期望的保护作用，但是独立于NF-κ B，将留下通过调节NF-κ B的活化来干扰促炎基因上调的选择。
Endothelial cells (EC) play a key role in the propagation of inflammatory responses. Better understanding of inflammatory processes in EC might provide new ways of controlling inflammation. We report here that the known antioxidant pyrrolidinedithiocarbamate (PDTC) leads to time and dose dependent activation of heat-shock protein 70 (Hsp70) as well as Hsp32 in EC. We further demonstrate that PDTC activates heat-shock factor 1 (HSF1), one of several transcription factor involved in the upregulation of heat-shock proteins. And more importantly, we demonstrate that Hsp32 as well as Hsp70 can be upregulated independently of the transcription factor nuclear factor kappaB (NF-kappa B). The presented data provide further insight into the mechanism of Hsp32 and Hsp70 regulation, as well as further distinguishing these genes from other so called 'protective genes' whose upregulation depends on the activation of NF-kappa B. These findings indicate that Hsp32 and Hsp70 might be ideal candidates among protective genes. Hsp32 and Hsp70 provide many desirable protective effects but, being independent of NF-kappa B, would leave open the option to interfere with the upregulation of proinflammatory genes by modulating the activation of NF-kappa B.