Inhibition of endoplasmic reticulum stress alleviates lipopolysaccharide-induced lung inflammation through modulation of NF-κB/HIF-1α signaling pathway.
Inhibition of endoplasmic reticulum stress alleviates lipopolysaccharide-induced lung inflammation through modulation of NF-κB/HIF-1α signaling pathway.
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DOI：
10.1038/srep01142
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发表时间：
2013
影响因子：
4.6
通讯作者：
Lee, Yong Chul
中科院分区：
文献类型：
--
作者：
Kim, Hee Jung;Jeong, Jae Seok;Kim, So Ri;Park, Seung Yong;Chae, Han Jung;Lee, Yong Chul
脂多糖（LPS）参与多种炎性疾病。在应激条件下，内质网（内质网）功能失去稳态，即内质网应激。ER应激如何参与LPS诱导的肺部炎症尚不清楚。在这项研究中，ER应激抑制LPS诱导的肺部炎症和转录调控的影响进行了检查。ER应激调节剂4-苯基丁酸酯（PBA）可减少LPS诱导的肺中各种ER应激标志物的增加。此外，抑制ER应激可减轻LPS诱导的肺部炎症。抑制ER应激可降低LPS诱导的NF-κB和HIF-1α活性的升高。这些结果提示抑制ER应激可通过调节NF-κB/IκB和HIF-1α信号通路减轻LPS诱导的肺炎症反应。
Lipopolysaccharide (LPS) is involved in a variety of inflammatory disorders. Under stress conditions, endoplasmic reticulum (ER) loses the homeostasis in its functions, which is defined as ER stress. Little is known how ER stress is implicated in LPS-induced lung inflammation. In this study, effects of inhibition of ER stress on LPS-induced lung inflammation and transcriptional regulation were examined. An ER stress regulator, 4-phenylbutyrate (PBA) reduced LPS-induced increases of various ER stress markers in the lung. Furthermore, inhibition of ER stress reduced the LPS-induced lung inflammation. Moreover, LPS-induced increases of NF-κB and HIF-1α activity were lowered by inhibition of ER stress. These results suggest that inhibition of ER stress ameliorates LPS-induced lung inflammation through modulation of NF-κB/IκB and HIF-1α signaling pathway.
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影响因子：
14.2
作者：
Lee, Kyung Sun;Kim, So Ri;Lee, Yong Chul
通讯作者：
Lee, Yong Chul
影响因子：
4.4
作者：
Peyssonnaux, Carole;Cejudo-Martin, Pilar;Nizet, Victor
通讯作者：
Nizet, Victor
内质网应激与视网膜炎症和糖尿病性视网膜病有关。
影响因子：
3.5
作者：
Li, Jingming;Wang, Joshua J.;Yu, Qiang;Wang, Min;Zhang, Sarah X.
通讯作者：
Zhang, Sarah X.
DOI：
10.1164/rccm.200909-1427so
发表时间：
2010-06-15
影响因子：
24.7
作者：
Opitz, Bastian;van Laak, Vincent;Suttorp, Norbert
通讯作者：
Suttorp, Norbert
影响因子：
4
作者：
Semenza, GL
通讯作者：
Semenza, GL