| Project/Area Number |
16H06740
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Veterinary medical science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Kaji Noriyuki 東京大学, 大学院農学生命科学研究科(農学部), 助教 (20779318)
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| Project Period (FY) |
2016-08-26 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | カハール介在細胞 / ICC / 可塑性 / 一酸化窒素 / 消化管 / 炎症 / 消化管運動 / 腸炎 / 組織修復・再生 / 間葉系細胞 |
|---|
| Outline of Final Research Achievements |
The reporter protein was expressed in the interstitial cells of Cajal (ICC) but also intestinal smooth muscle cells in ANO1-Cre; reporter mice. This result suggests that common precursor cell of ICC and smooth muscle cell express ANO1. The most of c-Kit-positive ICC at the myenteric plexus layer were also positive for AIC, an antibody for ICC. However, some of AIC-positive cells did not express c-Kit although the cells were connected with c-Kit-positive ICC networks. Since AIC-positive cells were retained, compared with other ICC markers, in the smooth muscle layer obtained from postoperative ileus model mouse, it was suggested that AIC could be a marker of dedifferentiated ICC.Treatment of cultured ICC with low concentration of nitric oxide (NO) donor promote the growth of ICC networks. On the other hand, treatment with high concentration of NO donor decreased c-Kit-positive ICC. This result suggest that NO is key molecule to regulate the fate of ICC.
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