Reduced prosaposin levels in HepG2 cells with long-term coenzyme Q10 deficiency
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- Takeuchi Hikaru
- School of Bionics, Tokyo University of Technology
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- Sugawara Kyosuke
- School of Bionics, Tokyo University of Technology
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- Okamoto Mizuho
- School of Bionics, Tokyo University of Technology
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- Nakamura Akari
- School of Bionics, Tokyo University of Technology
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- Tanaka Tsukika
- School of Bionics, Tokyo University of Technology
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- Fujita Yui
- School of Bionics, Tokyo University of Technology
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- Ishiguro Kaiho
- School of Bionics, Tokyo University of Technology
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- Yamazaki Hana
- School of Bionics, Tokyo University of Technology
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- Okada Maiko
- School of Bionics, Tokyo University of Technology
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- Mikami Akane
- School of Bionics, Tokyo University of Technology
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- Fujisawa Akio
- School of Bionics, Tokyo University of Technology
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- Yamamoto Yorihiro
- School of Bionics, Tokyo University of Technology
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- Kashiba Misato
- School of Bionics, Tokyo University of Technology
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抄録
<p>Glycosphingolipids are involved in intercellular signaling, adhesion, proliferation, and differentiation. Saposins A, B, C, and D are cofactors required for glycosphingolipid hydrolysis. Saposins A–D are present in series in a common precursor protein, prosaposin. Thus, glycosphingolipids amounts depend on prosaposin cellular levels. We previously reported that prosaposin and saposin B bind coenzyme Q10 in human cells. Coenzyme Q10 is an essential lipid of the mitochondrial electron transport system, and its reduced form is an important antioxidant. Coenzyme Q10 level decrease in aging and in various progressive diseases. Therefore, it is interesting to understand the cellular response to long-term coenzyme Q10 deficiency. We established a long-term coenzyme Q10 deficient cell model by using the coenzyme Q10 biosynthesis inhibitor, 4-nitrobenzoate. The levels of coenzyme Q10 were reduced by 4-nitrobenzoate in HepG2 cells. Administration of 4-nitrobenzoate also decreased prosaposin protein and mRNA levels. The cellular levels of coenzyme Q10 and prosaposin were recovered by treatment with 4-hydroxybenzoquinone, a substrate for coenzyme Q10 synthesis that counteracts the effect of 4-nitrobenzoate. Furthermore, the ganglioside levels were altered in 4-nitrobenzoate treated cells. These results imply that long-term coenzyme Q10 deficiency reduces cellular prosaposin levels and disturbs glycosphingolipid metabolism.</p>
収録刊行物
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- Journal of Clinical Biochemistry and Nutrition
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Journal of Clinical Biochemistry and Nutrition 71 (2), 97-102, 2022
一般社団法人 日本酸化ストレス学会
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詳細情報 詳細情報について
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- CRID
- 1390011793671986304
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- ISSN
- 18805086
- 09120009
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
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- 抄録ライセンスフラグ
- 使用不可