| Project/Area Number |
15K11283
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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 |
Surgical dentistry
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| Research Institution | Osaka Dental University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MASUTANI Mitsuko 長崎大学, 大学院医歯薬学総合研究科・フロンティア生命科学分野, 教授 (60238904)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 再生医学 / 幹細胞 / エクソソーム / microRNA / 次世代シークエンス / miRNA / 細胞外RNA / 機能性RNA |
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| Outline of Final Research Achievements |
While the functions of Parp1 in intracellular signaling have been extensively studied, its roles in intercellular signaling remain to be established. In the present study, we used the Parp1-/- embryonic stem (ES) cell line, 210-58 established from the wild-type (Parp1+/+) ES cell line, J1. To examine whether Parp1 has roles in differentiation, cell growth, cell death, and other physiological processes by regulating intercellular communications, we compared the properties of microRNAs in exosomes derived from Parp1-/- and Parp1+/+ ES cells. Parp1 deficiency in ES cells led to inhibition of cell-cell communication, possibly by intercellular signal transduction, suggesting that Parp1 functions extracellularly by regulating exosomal microRNAs.
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