WEKO3
アイテム
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We recently found that the level of serum sulfatides was significantly lower in hemodialysis patients than that in normal subjects, and that the m serum level closely correlated to the incidence of cardiovascular disease. These findings suggest a relationship between the level of serum sulfatides and kidney function; however, the molecular mechanism underlying this relationship remains unclear. In the present study, the influence of kidney dysfunction on the metabolism of sulfatides was examined using an established murine model of acute kidney injury, protein-overload nephropathy in mice. Protein-overload treatment caused severe proximal tubular injuries within 4 days, and this treatment obviously decreased both serum and hepatic sulfatide levels. The sphingoid composition of serum sulfatides was very similar to that of hepatic ones at each time point, suggesting that the serum sulfatide level is dependent on the hepatic secretory ability of sulfatides. The treatment also decreased hepatic expression of cerebroside sulfotransferase (CST), a key enzyme in sulfatide metabolism, while it scarcely influenced the expression of the other sulfatide-metabolizing enzymes, including arylsulfatase A, ceramide galactosyltransferase, and galactosylceramidase. Pro-inflammatory responses were not detected in the liver of these mice: however, potential oxidative stress was increased. These results suggest that down-regulation of hepatic CST expression, probably affected by oxidative stress from kidney injury, causes reduction in liver and serum sulfatide levels. This novel mechanism, indicating the crosstalk between kidney injury and specific liver function, may prove useful for helping to understand the situation where human hemodialysis patients have low levels of serum sulfatides. (C) 2009 Elsevier Inc. 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Acute kidney injury induced by protein-overload nephropathy down-regulates gene expression of hepatic cerebroside sulfotransferase in mice, resulting in reduction of liver and serum sulfatides
http://hdl.handle.net/10091/10814
http://hdl.handle.net/10091/108143bc81e5c-1983-4195-97a6-1083584ab112
名前 / ファイル | ライセンス | アクション |
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2010-12-02 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Acute kidney injury induced by protein-overload nephropathy down-regulates gene expression of hepatic cerebroside sulfotransferase in mice, resulting in reduction of liver and serum sulfatides | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Sulfatides | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Sphingoglycolipids | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Acute kidney injury | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Protein-overload nephropathy | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Peroxisome proliferator-activated receptor | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | alpha (Ppara)-null mice | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Cerebroside sulfotransferase (CST) | |||||
資源タイプ | ||||||
資源 | http://purl.org/coar/resource_type/c_6501 | |||||
タイプ | journal article | |||||
著者 |
Zhang, Xiaowei
× Zhang, Xiaowei× Nakajima, Takero× Kamijo, Yuji× Li, Gang× Hu, Rui× Kannagi, Reiji× Kyogashima, Mamoru× Aoyama, Toshifumi× Hara, Atsushi |
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信州大学研究者総覧へのリンク | ||||||
氏名 | Nakajima, Takero | |||||
URL | http://soar-rd.shinshu-u.ac.jp/profile/ja.ymTNuNkh.html | |||||
信州大学研究者総覧へのリンク | ||||||
氏名 | Kamijo, Yuji | |||||
URL | http://soar-rd.shinshu-u.ac.jp/profile/ja.gCTFuakh.html | |||||
出版者 | ||||||
出版者 | ACADEMIC PRESS INC ELSEVIER SCIENCE | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS. 390(4):1382-1388 (2009) | |||||
書誌情報 |
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 巻 390, 号 4, p. 1382-1388, 発行日 2009-12-25 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Sulfatides, possible antithrombotic factors belonging to sphingoglycolipids, are widely distributed in mammalian tissues and serum. We recently found that the level of serum sulfatides was significantly lower in hemodialysis patients than that in normal subjects, and that the m serum level closely correlated to the incidence of cardiovascular disease. These findings suggest a relationship between the level of serum sulfatides and kidney function; however, the molecular mechanism underlying this relationship remains unclear. In the present study, the influence of kidney dysfunction on the metabolism of sulfatides was examined using an established murine model of acute kidney injury, protein-overload nephropathy in mice. Protein-overload treatment caused severe proximal tubular injuries within 4 days, and this treatment obviously decreased both serum and hepatic sulfatide levels. The sphingoid composition of serum sulfatides was very similar to that of hepatic ones at each time point, suggesting that the serum sulfatide level is dependent on the hepatic secretory ability of sulfatides. The treatment also decreased hepatic expression of cerebroside sulfotransferase (CST), a key enzyme in sulfatide metabolism, while it scarcely influenced the expression of the other sulfatide-metabolizing enzymes, including arylsulfatase A, ceramide galactosyltransferase, and galactosylceramidase. Pro-inflammatory responses were not detected in the liver of these mice: however, potential oxidative stress was increased. These results suggest that down-regulation of hepatic CST expression, probably affected by oxidative stress from kidney injury, causes reduction in liver and serum sulfatide levels. This novel mechanism, indicating the crosstalk between kidney injury and specific liver function, may prove useful for helping to understand the situation where human hemodialysis patients have low levels of serum sulfatides. | |||||
資源タイプ(コンテンツの種類) | ||||||
内容記述タイプ | Other | |||||
内容記述 | Article | |||||
ISSN | ||||||
収録物識別子タイプ | PISSN | |||||
収録物識別子 | 0006-291X | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00564395 | |||||
PubMed | ||||||
識別子タイプ | PMID | |||||
関連識別子 | https://pubmed.ncbi.nlm.nih.gov/19895791 | |||||
関連名称 | 19895791 | |||||
DOI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1016/j.bbrc.2009.10.164 | |||||
関連名称 | 10.1016/j.bbrc.2009.10.164 | |||||
権利 | ||||||
権利情報 | Copyright (c) 2009 Elsevier Inc. | |||||
出版タイプ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
WoS | ||||||
表示名 | Web of Science | |||||
URL | http://gateway.isiknowledge.com/gateway/Gateway.cgi?&GWVersion=2&SrcAuth=ShinshuUniv&SrcApp=ShinshuUniv&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000272650800056 |