Trehalose activates autophagy and decreases proteasome inhibitor‐induced endoplasmic reticulum stress and oxidative stress‐mediated cytotoxicity in hepatocytes
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- Yuichi Honma
- Third Department of Internal Medicine University of Occupational and Environmental Health Kitakyushu Japan
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- Miyuki Sato‐Morita
- Third Department of Internal Medicine University of Occupational and Environmental Health Kitakyushu Japan
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- Yuka Katsuki
- Third Department of Internal Medicine University of Occupational and Environmental Health Kitakyushu Japan
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- Hitomi Mihara
- Third Department of Internal Medicine University of Occupational and Environmental Health Kitakyushu Japan
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- Ryoko Baba
- Department of Anatomy, School of Medicine University of Occupational and Environmental Health Kitakyushu Japan
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- Masaru Harada
- Third Department of Internal Medicine University of Occupational and Environmental Health Kitakyushu Japan
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説明
<jats:sec><jats:title>Aim</jats:title><jats:p>Endoplasmic reticulum stress is associated with the pathophysiology of various liver diseases. Endoplasmic reticulum stress mediates the accumulation of abnormal proteins and leads to oxidative stress, cytoplasmic inclusion body formation, and apoptosis in hepatocytes. Autophagy is a bulk degradation pathway for long‐lived cytoplasmic proteins or damaged organelles and is also a major degradation pathway for many aggregate‐prone and disease‐causing proteins. We previously reported that rapamycin, a mammalian target of rapamycin inhibitor, activated autophagy and decreased proteasome inhibitor‐mediated ubiquitinated protein accumulation, cytoplasmic inclusion body formation, and apoptosis in hepatocytes. Trehalose is a non‐reducing disaccharide that has been shown to activate autophagy. It has been reported to decrease aggregate‐prone proteins and ameliorate cytotoxicity in neurodegenerative disease models. However, the effects of trehalose in hepatocytes are unclear.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>We show here that trehalose activated autophagy and reduced endoplasmic reticulum stress, cytoplasmic inclusion body formation, and apoptosis in proteasome inhibitor‐treated liver‐derived cultured cells.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>To our knowledge, this is the first report showing that trehalose activates autophagy and has cytoprotective effects in hepatocytes. Our findings suggest that trehalose can become a therapeutic agent for endoplasmic reticulum stress‐related liver diseases.</jats:p></jats:sec>
収録刊行物
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- Hepatology Research
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Hepatology Research 48 (1), 94-105, 2017-05-04
Wiley
