| Project/Area Number |
25893192
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory medicine
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| Research Institution | Kagoshima University |
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Principal Investigator |
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| Research Collaborator |
HASHIGUCHI Teruto 鹿児島大学, 大学院医歯学総合研究科, 教授 (70250917)
SHIMIZU Toshiaki 鹿児島大学, 大学院医歯学総合研究科, 助教 (50468055)
OYAMA Yoko 鹿児島大学, 医学部・歯学部付属病院, 特任助教 (20583470)
TAKENOUCHI Kazunori 鹿児島大学, 医学部・歯学部付属病院, 医員 (30646758)
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| Project Period (FY) |
2013-08-30 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | マイクロRNA / 血小板 / 血管内皮細胞 / 糖尿病 / エクソゾーム / microRNA |
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| Research Abstract |
Diabetes is one of the major public health problem. Dysfunction of endothelial cells are involved in formation of the pathogenesis of this vascular diseases associated with diabetes. Our hypothesis is that cell to cell communication between endothelial cells and platelets would play a pivotal role in diabetic vascular complications. microRNAs (miRNAs) is a non-coding miRNAs that regulates protein synthesis post-transcriptionally. We used miRNAs as key players to organize a series of vascular events under hyperglycemia. We have discovered that miR-503 was induced by hypoxia in cultured endothelial cells and that miR-503 regulates phosphorylation of Akt as well as cyclin D. We also observed that miR-503 is released by wrapping in exosomes under hypoxic condition. In the future studies, we will focus on the downstream target of Akt regulated by miR-503 in endothelial cells and clarify the mechanisms by which endothelial cells transfer the information to platelets.
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