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KMID : 1034820150110020167
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Molecular & Cellular Toxicology
2015 Volume.11 No. 2 p.167 ~ p.174
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Crotonaldehyde-exposed macrophages induce heme oxygenase-1 expression as an adaptive mechanism
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Lee Seung-Eun
Yang Ha-Na
Son Gun-Woo
Park Hye-Rim
Jin Young-Ho
Park Cheung-Seog
Park Yong-Seek
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Abstract
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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.
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KEYWORD
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Heme oxygenase-1, Crotonaldehyde, Cigarette smoke, Macrophages, Adaptive response, Protective effect
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