| Project/Area Number |
26460390
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Kyoto University |
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Principal Investigator |
NODA MAKOTO 京都大学, 医学研究科, 教授 (30146708)
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUZAKI Tomoko 京都大学, 大学院医学研究科, 助教 (50402855)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 組織細胞 / 循環器・高血圧 / 生体分子 / 癌 / 発生・分化 / 組織・細胞 |
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| Outline of Final Research Achievements |
RECK has been characterized as a protein suppressing cancer metastasis/recurrence and downregulated in a wide variety of tumors. Reck-deficient mice, on the other hand, die at mid-gestation stage with arrested vascular development. Hence, studies on the physiological functions of RECK may yield important insights into the mechanisms of both vascular disorders and cancer progression. In this project, we attempted, by using genetically engineered mice and organ culture techniques, to elucidate the functions of RECK in two types of cells constituting blood vessels: vascular endothelial cells and mural cells. Our results indicate that mural RECK is required for mid-gestation cardiovascular development while endothelial RECK is essential for brain angiogenesis at a later developmental stage. Our data also indicate that RECK promotes the proper interactions between endothelial and mural cells essential for vascular stability.
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