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- MyD88 is a mediator for the activation of Nrf2 = MyD88에 의한 Nrf2 활성화
- 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
- 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.
- Gene regulationInflammationMacrophagesNrf2SiRNATLR4 signaling
- Appears in Collections:
- Ochang Branch Institute > 1. Journal Articles
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
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