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Motohiro Takeya
Department Kumamoto Health Science University Department of Medical Technology, Faculty of Health Science Position Professor |
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| Research Period | 2001～2002 |
| Research Topic | Roles of CD36 and SR-BI as novel AGE-receptors |
| Research Type | KAKENHI Research |
| Consignor | Ministry of Education, Culture, Sports, Science and Technology |
| Research Program Type | Grants-in-Aid for Scientific Research(基盤研究(B)),基盤研究(B) |
| KAKENHI Grant No. | 13470228 |
| Representative Person | Seikoh HORIUCHI |
| Collaborative Researcher | Motohiro TAKEYA |
| Details | In the Maillard reaction, the reaction of proteins with glucose or other reduced sugars leads, through the Schiff base and Amadori product, to the formation of advanced glycation endproducts (AGE). Recent studies of AGE-structures in vivo as well as the AGE-receptors have emphasized the involvement of post-translational AGE-modification in aging and age-enhanced disease processes such as diabetic complications and atherosclerosis. Three AGE-receptors such as SR-A (type A scavenger receptor), galectin-3 and RAGE (receptor tor AGE) were known. Our recent studies identified CD36 and SR-BI as novel AGE-receptors; CD36-overexpressed CHO cells showed endocytic uptake and subsequent intracellular degradation of AGE-proteins, suggesting that AGE-proteins ate recognized by CD36, which might contribute to the pathogenesis of diabetic vascular complications. By using SR-BI-overexpressed CHO cells (SR-BI-CHO), we showed that SR-BI-mediated selective uptake of cholesteryl esters of HDL as well as HDL-mediated cholesterol efflux from SR-BI-CHO cells were effectively inhibited by AGE-proteins, indicating that AGE-proteins play a significant role in HDL-mediated reverse cholesterolIn the present s |
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