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Title 

MyD88 is a mediator for the activation of Nrf2

 

MyD88에 의한 Nrf2 활성화

Authors 

K H KimJ H LyuS T KooSei Ryang OhHyeong Kyu LeeKyung Seop AhnR T SadikotM Joo

Publisher 

Elsevier

Issue Date 

2011

Citation 

Biochemical and Biophysical Research Communications, vol. 404, no. 1, pp. 46-51

Keywords 

Gene regulationInflammationMacrophagesNrf2SiRNATLR4 signaling

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.

ISSN 

0006-291X

Link 

http://dx.doi.org/10.1016/j.bbrc.2010.11.051

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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