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NRF2 and HSF1 coordinately regulate heme oxygenase-1 expression.

Sachiye Inouye1, Yuta Hatori2, Takanori Kubo2

  • 1Department of Pharmacy, Faculty of Pharmaceutical Sciences, Sanyo-Onoda City University, Japan.

Biochemical and Biophysical Research Communications
|October 15, 2018
PubMed
Summary

Heat shock factor 1 (HSF1) and nuclear factor-erythroid-2-related factor 2 (NRF2) suppress heme oxygenase-1 (HO-1) expression. HSF1 inhibits heme-induced HO-1, while NRF2 suppresses heat-induced HO-1 in mouse cells.

Keywords:
Heat shock factor 1 (HSF1)Heme oxygenase-1 (HO-1)Nuclear factor-erythroid-2-related factor 2 (NRF2)Stress response

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Area of Science:

  • Molecular Biology
  • Cellular Stress Response
  • Enzymology

Background:

  • Heme oxygenase-1 (HO-1), also known as heat shock protein 32, is a cytoprotective enzyme induced by various stresses.
  • The induction of HO-1 by heat shock is variable across species and cell types.
  • Understanding the regulatory mechanisms of HO-1 induction is crucial for its therapeutic potential.

Purpose of the Study:

  • To investigate the roles of heat shock factor 1 (HSF1) and nuclear factor-erythroid-2-related factor 2 (NRF2) in regulating heme oxygenase-1 (HO-1) expression.
  • To elucidate the distinct pathways involved in heme-induced versus heat-induced HO-1 expression.
  • To determine the suppressive roles of HSF1 and NRF2 on HO-1 induction.

Main Methods:

  • Utilized mouse embryonic fibroblast (MEF) cells deficient in HSF1 (Hsf1-/-) and NRF2 (Nrf2-/-).
  • Examined HO-1 mRNA and protein levels following induction by heme or heat shock (40-42°C).
  • Employed small interfering RNA (siRNA) to knockdown HSF1 in Nrf2-/- cells.

Main Results:

  • Heme-induced HO-1 expression was significantly higher (2-fold) in Hsf1-/- cells compared to wild-type cells.
  • Heme-induced HO-1 expression was undetectable in Nrf2-/- cells.
  • Heat shock markedly induced HO-1 in Nrf2-/- cells, whereas wild-type cells showed no response.
  • Heat-induced HO-1 expression in Nrf2-/- cells was abolished by HSF1 knockdown.

Conclusions:

  • HSF1 acts as a suppressor of heme-induced HO-1 expression.
  • NRF2 functions as a suppressor of heat-induced HO-1 expression.
  • These findings reveal distinct regulatory roles for HSF1 and NRF2 in controlling HO-1 expression under different stress conditions.