MyD88 is a mediator for the activation of Nrf2

Kyun Ha Kim, Ji Hyo Lyu, Sung Tae Koo, Sei Ryang Oh, Hyeong Kyu Lee, Kyung Seop Ahn, Ruxana T. Sadikot, Myungsoo Joo

Research output: Contribution to journalArticlepeer-review

20 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)46-51
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number1
StatePublished - Jan 7 2011
Externally publishedYes


  • Gene regulation
  • Inflammation
  • Macrophages
  • Nrf2
  • SiRNA
  • TLR4 signaling

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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