| Project/Area Number |
23592010
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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 |
Digestive surgery
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| Research Institution | The University of Tokushima |
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Principal Investigator |
IWATA Takashi 徳島大学, ヘルスバイオサイエンス研究部, 准教授 (00380022)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMADA Mitsuo 徳島大学, 大学院ヘルスバイオサイエンス研究部, 教授 (10216070)
UTSUNOMIYA Toru 徳島大学, 大学院ヘルスバイオサイエンス研究部, 准教授 (30304801)
KURITA Nobuhiro 徳島大学, 大学病院, 特任教授 (30335814)
IKEMOTO Tetsuya 徳島大学, 大学院ヘルスバイオサイエンス研究部, 助教 (20398019)
YOSHIKAWA Kozo 徳島大学, 大学院ヘルスバイオサイエンス研究部, 助教 (80448331)
西岡 将規 徳島大学, 大学病院, 助教 (50398020)
森本 慎也 徳島大学, 大学病院, 特任助教 (00548745)
東島 潤 徳島大学, 大学病院, 特任助教 (30467815)
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| Co-Investigator(Renkei-kenkyūsha) |
YASUTOMO Koji 徳島大学, 大学院ヘルスバイオサイエンス研究部, 教授 (30333511)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 膵島移植 / 拒絶反応 / 脂肪由来幹細胞 / 免疫寛容 / trophic効果 / homing効果 / OP9DL1細胞 / VEGF signal / 脂肪由来幹細胞（ADSC） / 調節性T細胞 Treg / helper T細胞 / suppressor T細胞 |
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| Research Abstract |
Cocultivation OP9-DL1 cell and human ADSC was performed, but pollution in culture enforced to take time. As an allied experiment, the cocultivation ADSC with the pancreatic islet, ADSC with hepatocytes, and the liver segmental resection+I/R+ ADSC, STZ injured pancreas+ADSC model were performed. Trophic effect and homing effect were investigated in remnant liver and injured pancreas.
Cocultivation: cell viability was high in both groups, and VEGF density was high prices out of the culture fluid in both groups. When anti VEGF antibody was added in culture fluid, pancreatic islet viabilty decreased. Thus it was thought that VEGF signal might be key signal of the pancreatic islet protection. In the liver segmental resection+I/R+ADSC model, ADSC showed homing in remnant liver. The hepatocytes with SDF-1appearance changed into non-substance cell. There was no homing of ADSC in STZ injured pancreas + ADSC model.ADSC showed organ-specifically trophic, homing, and a cell protection effect.
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