2015 Fiscal Year Final Research Report
The role of ERK5 in diabetic vascular calcification mediated by endothelial-to-mesenchymal transition
| Project/Area Number |
26860172
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General pharmacology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Keywords | 血管石灰化 / 内皮間葉転換 / ERK5 / スタチン |
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| Outline of Final Research Achievements |
First of all, we found that pitavastatin, one of lipid lowering agents, can activate ERK5 in endothelial cells by high throughput screening. Pitavastatin increased endothelial nitric oxide synthase (eNOS) expression via ERK5 activation. As eNOS was increased, VE-cadherin, a marker of endothelial cell, was also increased by pitavastatin treatment. NO generation is suggested to regulate VE-cadherin expression and play an important role in the maintain of endothelial cell character. Therefore, it was suggested that pitavastatin might prevent endothelial cells from endothelium-to-mesenchymal transition via ERK5 activation-eNOS expression-NO generation pathway.
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| Free Research Field |
薬理学
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