| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
In the present study, we have succeeded to establish a novel acute aortic dissection model mouse. Aortic dissection in C57Bl/6J mouse is induced by the combined usage of Nω-nitro-L-arginine methyl ester (L-NAME), angiotensin II (Ang II), and β-aminopropionitrile (BAPN). L-NAME induces endothelial cell damage. Administration of Ang II elevated systolic blood pressure. BAPN is one of the lysyloxidase inhibitor, which causes vessel medial fragility. We named this model “LAB” model. Pitavastatin, an HMG-CoA inhibitor used as lipid lowering agent, suppressed the incidence of aortic dissection. From the results of in vitro analysis using cultured human umbilical vein endothelial cells, pitavastatin effects are mediated by extracellular signal-regulated kinase 5 (ERK5) activation. Our findings suggested that this novel “LAB” model are useful to examine the pathophysiology of aortic dissection and the estimation of the drug efficacy against aortic dissection.
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