The molecular mechanisms underlying release and signaling of microparticle in the vascular diseases of diabetic states.
Project/Area Number |
15K07975
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pharmacology in pharmacy
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Research Institution | Hoshi University |
Principal Investigator |
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Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | 血管機能障害 / マイクロパーテイクル / 細胞外小胞 / 糖尿病 / 血管機能 / マイクロパーティクル / 血管内皮細胞 / 血管障害 / 内皮細胞機能 / アンギオテンシン / 高血糖 / 内皮機能 / 血小板 |
Outline of Final Research Achievements |
Microparticles (MPs) have been described as biological vectors of vascular diseases in other pathologies. I investigated the role of MPs derived from diabetic states in vascular diseases. I found that circulating MPs isolated from diabetic rats impair the endothelial function in response to ACh by directly reducing eNOS expression in carotid arteries. The results strongly suggest that MPs affect endothelial NO vasorelaxation by regulating the protein expressions of eNOS and caveolin-1. I found that high glucose and Ang II directly affect endothelial cells and the production of MPs and indicate involvement of a novel ERK1/2 pathway; the resultant MPs aggravate endothelial dysfunction by regulating eNOS protein levels and ERK1/2 signalling in mice aortas. Reducing numbers of circulating MPs or blocking their effects by inhibiting ERK1/2 activation may offer effective therapeutic approaches for treating endothelial dysfunction in diabetes patients.
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Report
(4 results)
Research Products
(104 results)
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[Journal Article] Pioglitazone Ameliorates Smooth Muscle Cell Proliferation in Cuff-Induced Neointimal Formation by Both Adiponectin-Dependent and -Independent Pathways.2016
Author(s)
Kubota T, Kubota N, Sato H, Inoue M, Kumagai H, Iwamura T, Takamoto I, Kobayashi T, Moroi M, Terauchi Y, Tobe K, Ueki K, Kadowaki T
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Journal Title
Sci Rep
Volume: 6
Issue: 1
Pages: 34707-34707
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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