Roles of S100B Protein in Diabetic Nephropathy
| Autor: | Chao-Tang Chuang, 莊詔棠 |
|---|---|
| Rok vydání: | 2009 |
| Druh dokumentu: | 學位論文 ; thesis |
| Popis: | 97 Diabetic nephropathy（DN） is diabetes patient''s common complication and cause of mortality. It’s pathologic phenomenon is kidney cell proliferation、hypertrophy、accumulation of extracellular matrix, which leads to renal fibrosis and end-stage renal disease(ESRD). High glucose, advanced glycation end products(AGEs)and TGF-β1 are important in the pathogenesis of DN. In previous studies, high glucose induces renal tubular hypertrophy and affects the structure and function of renal mesangial cells. AGEs lead to renal disease via receptor for advanced glycation end products(RAGE), S100B also binds to RAGE. S100B induces cell proliferation in vascular smooth muscle cells, and induces inflammation and TGF-β expression. In this study, we found that high glucose induced S100B expression in mouse mesangial cells(Mes 13 cell line). S100B induced cyclin D1 protein expression via the p38 MAPK and JNK pathway and induced cell proliferation at 4 hours. In long term, S100B induced p21 expression via the TGF-β/Smad pathway and induced hypertrophy at 1 day. S100B induced accumulation of extracellular matrix protein, collagen type IV and Fibroectin, decreased cell adhesion protein, E-cadherin. S100B also 11 induced inflammation factors, NF-κB、COX-2、AP1 expression. S100B protein expression was increased in the kidney of the streptozotocin diabetic rats. We conclude that S100B maybe involved in the process of DN in vitro and in vivo. |
| Databáze: | Networked Digital Library of Theses & Dissertations |
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