| Project/Area Number |
16K10436
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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 |
General surgery
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| Research Institution | University of the Ryukyus |
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Principal Investigator |
Kurima Kiyoto 琉球大学, 医学部, 委託非常勤講師 (10755713)
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| Co-Investigator(Kenkyū-buntansha) |
潮平 知佳 琉球大学, 医学(系)研究科(研究院), 助教 (50325833)
野口 洋文 琉球大学, 医学(系)研究科(研究院), 教授 (50378733)
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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: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | p38MAPK / アポトーシス / 蛋白導入システム / ペプチド / 膵島移植 / p38MARK / 膵島細胞 / 抗アポプトーシスペプチド |
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| Outline of Final Research Achievements |
Here we synthesized peptides to inhibit p38, which were derived from the sites on p38 that mediate binding to proteins such as MAPK kinases (MKKs). The p38 inhibitory peptides (p38I) significantly inhibited the activation of p38. To evaluate the effects of p38I, mouse and porcine islets were incubated with 10 micromole p38I. After culture, the numbers of islets in the p38I-treated cultures were significantly higher compared with those of cultures treated with control peptide. After islet transplantation, blood glucose levels reached the normoglycemic range in 58.3% and 0% of diabetic mice treated with p38I or control peptide, respectively. These data suggest that p38I inhibited islet apoptosis and improved islet function.
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| Academic Significance and Societal Importance of the Research Achievements |
p38MAPKの抑制薬は、研究試薬として様々な実験に使用されるのみならず、膵島の抗アポトーシスペプチドとして臨床応用化することも期待できる。また、この方法が確立されれば、他の抑制剤も同様の手法によって作成が可能となるため、本研究は新規性が高く、独創的で画期的な研究であると考えられる。
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