MyD88 is a mediator for the activation of Nrf2 = MyD88에 의한 Nrf2 활성화

Cited 20 time in scopus
Metadata Downloads
Title
MyD88 is a mediator for the activation of Nrf2 = MyD88에 의한 Nrf2 활성화
Author(s)
K H Kim; J H Lyu; S T Koo; Sei Ryang Oh; Hyeong Kyu Lee; Kyung Seop Ahn; R T Sadikot; M Joo
Bibliographic Citation
Biochemical and Biophysical Research Communications, vol. 404, no. 1, pp. 46-51
Publication Year
2011
Abstract
If not controlled properly, inflammatory response is often detrimental. However, in many cases, it can be self-limited and subsides without inflicting tissue damage. In this study, we tested the hypothesis that inflammatory stimuli can trigger anti-inflammatory response, which may contribute to limiting tissue damage induced by excessive inflammation. We found that treatment of bone marrow-derived macrophages with lipopolysaccharide (LPS) activated NF-E2-related factor 2 (Nrf2), a basic leucine zipper transcription factor that regulates inflammation, leading to expression of Nrf2-regulated genes including NAD(P)H:quinine oxidoreductase 1,glutamyl cysteine ligase catalytic unit and heme oxygenase-1. Suppression of Nrf2 by siRNA significantly diminished the expression of the Nrf2-regulated genes induced by LPS. By using pharmacological, genetic and epigenetic analyses, we found that activation of Nrf2 in response to LPS is dependent on MyD88 but independent of the production of reactive oxygen species. Together, our results show that activation of Nrf2 by MyD88 dependent signaling induced by LPS is an important intrinsic mechanism that limits excessive inflammation.
Keyword
Gene regulationInflammationMacrophagesNrf2SiRNATLR4 signaling
ISSN
0006-291X
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.bbrc.2010.11.051
Type
Article
Appears in Collections:
Ochang Branch Institute > 1. Journal Articles
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.