Crotonaldehyde-exposed macrophages induce heme oxygenase-1 expression as an adaptive mechanism

Seung Eun Lee, Hana Yang, Gun Woo Son, Hye Rim Park, Young Ho Jin, Cheung Seog Park, Yong Seek Park

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

Cigarette smoke represents one of the most significant risk factors for the progression of vascular disease. Exposure to cigarette smoke induces oxidative stress in the vascular system and results in vascular dysfunction. Crotonaldehyde, a highly reactive α, β-unsaturated aldehyde, is a foremost compound of cigarette smoke and a product of endogenous lipid peroxidation. Heme oxygenase-1 (HO-1) expression plays an essential role in cellular defense against environmental insults and represents an adaptive response. Here, we showed the effects of crotonaldehyde on the induction of HO-1 expression in RAW 264.7 macrophages. Crotonaldehyde treatment resulted in significantly increased phosphorylation of p38 mitogen-activated protein kinase (MAPK) and nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2). Furthermore, treatment with zinc protoporphyrin (ZnPP; the specific HO-1 inhibitor) markedly augmented the death of crotonaldehyde-treated macrophages. In summary, these results highlight the role of the HO-1 upregulation through p38 MAPK-Nrf2 activation in the adaptive response to crotonaldehyde in macrophages.

Original languageEnglish (US)
Pages (from-to)167-174
Number of pages8
JournalMolecular and Cellular Toxicology
Volume11
Issue number2
DOIs
StatePublished - Jun 1 2015

Keywords

  • Adaptive response
  • Cigarette smoke
  • Crotonaldehyde
  • Heme oxygenase-1
  • Macrophages
  • Protective effect

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