Investigation of the mechanism of vasculitis and atherosclerosis in autoinflammatory disease using iPS cell
| Project/Area Number |
15K19622
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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 |
Pediatrics
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 自己炎症性疾患 / 動脈硬化 / CINCA症候群 / NLRP3 inflammasome / iPS細胞 / 血管内皮細胞 / 血管平滑筋細胞 |
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| Outline of Final Research Achievements |
We established a system of differentiation into vascular endothelial cells (EC) and vascular smooth muscle cells (VSMC) from iPS cells of patients with CINCA syndrome. Differentiated cells had discriminative markers. EC had functions of tube formation and cytokine production. We stimulated the NLRP3 inflammasome of the obtained cells with LPS and TNFα(priming signal), ATP and silica(activation signal). There was no significant difference in production of the inflammatory cytokines and adhesion molecules between the differentiated cells from mutant iPS cells and wild-type iPS cells. NLRP3 expression in EC and VSMC from iPS cells was scarce compared with primary cells such as HUVEC and HASMC. Further study is needed to reevaluate the differentiation system, and to investigate the functions of the NLRP3 inflammasome in primary cells.
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Report
(3 results)
Research Products
(2 results)
