| Halofuginone prevents extracellular matrix deposition in diabetic nephropathy. | |
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MedLine Citation:
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PMID: 19114027 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Transforming growth factor-beta (TGF-beta) is known to promote the accumulation of extracellular matrix (ECM) and the development of diabetic nephropathy. Halofuginone, an analog of febrifugine, has been shown to block TGF-beta(1) signaling and subsequent type I collagen production. Here, the inhibitory effect of halofuginone on diabetic nephropathy was examined. Halofuginone suppressed Smad2 phosphorylation induced by TGF-beta(1) in cultured mesangial cells. In addition, the expression of TGF-beta type 2 receptor decreased by halofuginone. Halofuginone showed an inhibitory effect on type I collagen and fibronectin expression promoted by TGF-beta(1). An in vivo experiment using db/db mice confirmed the ability of halofuginone to suppress mesangial expansion and fibronectin overexpression in the kidneys. Moreover, an analysis of urinary 8-OHdG level and dihydroethidium fluorescence revealed that halofuginone reduced oxidative stress in the glomerulus of db/db mice. These data indicate that halofuginone prevents ECM deposition and decreases oxidative stress, thereby suppressing the progression of diabetic nephropathy. |
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Authors:
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Seiya Sato; Harukiyo Kawamura; Minoru Takemoto; Yoshiro Maezawa; Masaki Fujimoto; Tatsushi Shimoyama; Masaya Koshizaka; Yuya Tsurutani; Aki Watanabe; Shiro Ueda; Karin Halevi; Yasushi Saito; Koutaro Yokote |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-12-27 |
Journal Detail:
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Title: Biochemical and biophysical research communications Volume: 379 ISSN: 1090-2104 ISO Abbreviation: Biochem. Biophys. Res. Commun. Publication Date: 2009 Feb |
Date Detail:
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Created Date: 2009-01-21 Completed Date: 2009-02-13 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0372516 Medline TA: Biochem Biophys Res Commun Country: United States |
Other Details:
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Languages: eng Pagination: 411-6 Citation Subset: IM |
Affiliation:
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Department of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Collagen Type I / antagonists & inhibitors, metabolism Diabetic Nephropathies / metabolism*, pathology* Extracellular Matrix / drug effects*, pathology* Fibronectins / antagonists & inhibitors, metabolism Mesangial Cells / drug effects, metabolism, pathology Mice Mice, Inbred Strains Oxidative Stress / drug effects Piperidines / pharmacology* Quinazolinones / pharmacology* Rats Smad2 Protein / metabolism Transforming Growth Factor beta / antagonists & inhibitors |
| Chemical | |
Reg. No./Substance:
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0/Collagen Type I; 0/Fibronectins; 0/Piperidines; 0/Quinazolinones; 0/Smad2 Protein; 0/Transforming Growth Factor beta; 17395-31-2/halofuginone |
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