Iron deficiency induces autophagy and activates Nrf2 signal through modulating p62/SQSTM
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- INOUE Hirofumi
- Department of Nutritional Science and Food Safety, Tokyo University of Agriculture
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- HANAWA Nobuaki
- Department of Nutritional Science, Faculty of Applied Bioscience, Tokyo University of Agriculture
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- KATSUMATA Shin-Ichi
- Department of Nutritional Science, Faculty of Applied Bioscience, Tokyo University of Agriculture
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- KATSUMATA-TSUBOI Rie
- Department of Nutritional Science and Food Safety, Tokyo University of Agriculture
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- TAKAHASHI Nobuyuki
- Department of Nutritional Science and Food Safety, Tokyo University of Agriculture
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- UEHARA Mariko
- Department of Nutritional Science and Food Safety, Tokyo University of Agriculture
書誌事項
- タイトル別名
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- <b>Iron deficiency induces autophagy and activates Nrf2 signal through modulating </b><b>p62/SQSTM </b>
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説明
<p>Iron is an essential trace metal in almost all organisms and plays an important role in the redox system. We previously reported that iron deficiency activated autophagy and nuclear factor erythroid 2-related factor 2 (Nrf2) signaling for oxidative stress. However, regulatory mechanisms underlying the association between autophagy and Nrf2 signaling are unclear. In this study, we found that treatment of cells with an iron-specific chelator deferoxamine (DFO) increased reactive oxidative species (ROS) production by elevating the expression of p47phox and p67phox compared with that in untreated cells. The DFO treatment also induced protein aggregation and formed aggresome, which is a cellular response to misfolded protein. In addition, DFO treatment upregulated the expression of the autophagic gene p62/SQSTM1, which in turn activated intracellular proteolysis during autophagy. DFO treatment phosphorylated p62/SQSTM1 (Thr351) to activate Nrf2. However, silencing of p62/SQSTM1 followed by DFO treatment attenuated Nrf2 activation and resulted in the accumulation of carboxyl proteins compared with DFO treatment alone. These results indicated that iron deficiency activates Nrf2 signaling by modulating p62/SQSTM1 during autophagy.</p>
収録刊行物
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- Biomedical Research
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Biomedical Research 38 (6), 343-350, 2017
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