| Project/Area Number |
16K09498
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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 |
Cardiovascular medicine
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
桑原 宏一郎 信州大学, 学術研究院医学系, 教授 (30402887)
錦見 俊雄 京都大学, 医学研究科, 非常勤講師 (80291946)
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| Research Collaborator |
MINAMINO NAOTO 国立研究開発法人 国立循環器病研究センター
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 糖鎖修飾 / proBNP / 糖鎖 / 分子心臓病学 / 循環器・高血圧 |
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| Outline of Final Research Achievements |
BNP is secreted from the heart and is a cardioprotective peptide, but its precursor proBNP is present in the blood and its biological activity is extremely weak compared to BNP. However, the secretion mechanism of this proBNP was unknown. In this study, we suggested that miR-30, a microRNA abundant in the heart, regulates the gene expression of the O-linked glycosyltransferases, GALNT1 and GALNT2, in a repressive manner, thereby regulating the glycosylation of proBNP by GALNT1 and GANT2, and that miR-30-GALNT pathway is involved in the glycosylation-dependent regulation of the processing and secretion of proBNP.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究により、低活性のproBNP分泌メカニズムの一端が明らかとなり、これらの分子メカニズムを修飾することで、心不全の新たな診断法や、活性の強いBNPの分泌が促進されるような新たな心不全治療の開発につながる可能性が有る意義のある研究成果が得られたと考える。
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