徳島大学 教育・研究者情報データベース(EDB)

1. (英) Ohashi Seiji / (日) 大橋 誠治 / (読) おおはし せいじ

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2. 安部 秀斉

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3. (英) Takahashi Toshikazu / (日) 高橋 利和 / (読) たかはし としかず

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4. (英) Yamamoto Yasuhiko

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5. (英) Takeuchi Masayoshi

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6. (英) Arai Hidenori

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7. (英) Nagata Kazuhiro

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8. (英) Kita Toru

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9. (英) Okamoto Hiroshi

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10. (英) Yamamoto Hiroshi

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11. 土井 俊夫

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(英) Advanced glycation end products increase collagen-specific chaperone protein in mouse diabetic nephropathy

(英) Advanced glycation end products (AGEs) appear to contribute to the diabetic complications. This study reports the inhibitory effect of OPB-9195 (OPB), an inhibitor of AGEs formation, and the role of a collagen-specific molecular chaperone, a 47-kDa heat shock protein (HSP47) in diabetic nephropathy. Transgenic mice carrying nitric-oxide synthase cDNA fused with insulin promoter (iNOSTg) leads to diabetes mellitus. The iNOSTg mice at 6 months of age represented diffuse glomerulosclerosis, and the expression of HSP47 was markedly increased in the mesangial area in parallel with increased expression of types I and IV collagens. OPB treatment ameliorated glomerulosclerosis in the iNOSTg mice associated with the decreased expression of HSP47 and types I and IV collagens. The expression of transforming growth factor-beta (TGF-beta) was increased in glomeruli of iNOSTg mice and decreased after treatment with OPB. To confirm these mechanisms, cultured mesangial cells were stimulated with AGEs. AGEs significantly increased the expression of HSP47, type IV collagen, and TGF-beta mRNA. Neutralizing antibody for TGF-beta inhibited the overexpression of both HSP47 and type IV collagen in vitro. In conclusion, AGEs increase the expression of HSP47 in association with collagens, both in vivo and in vitro. The processes may be mediated by TGF-beta.

1. (英) Animals
2. (英) Blood Glucose
3. (英) Blotting, Western
4. (英) Cells, Cultured
5. コラーゲン(collagen)
6. (英) DNA-Binding Proteins
7. (英) Diabetic Nephropathies
8. (英) Glomerular Mesangium
9. (英) Glycosylation End Products, Advanced
10. (英) HSP47 Heat-Shock Proteins
11. (英) Heat-Shock Proteins
12. インスリン(insulin)
13. (英) Kidney
14. (英) Lasers
15. (英) Male
16. (英) Mice
17. (英) Mice, Inbred C57BL
18. (英) Mice, Transgenic
19. (英) Microscopy, Fluorescence
20. (英) Oligonucleotides, Antisense
21. (英) Polymerase Chain Reaction
22. (英) Promoter Regions, Genetic
23. (英) RNA, Messenger
24. (英) RNA, Small Interfering
25. (英) Ribonucleases
26. (英) Smad Proteins
27. (英) Thiadiazoles
28. (英) Thiazolidines
29. (英) Time Factors
30. (英) Trans-Activators
31. (英) Transfection
32. (英) Transforming Growth Factor beta

1. (英) Article.Affiliation: Department of Clinical Biology and Medicine, Course of Biological Medicine, School of Medicine, The University of Tokushima, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.

2. (英) Article.PublicationTypeList.PublicationType: Journal Article

3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't