| Project/Area Number |
10670503
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | AKITA UNIVERSITY (1999)
Juntendo University (1998) |
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Principal Investigator |
WATANABE Sumio School of Medicine, Akita University, Professor, 医学部, 教授 (20138225)
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| Co-Investigator(Kenkyū-buntansha) |
OTAKA Michiro School of Medicine, Akita University, Assistant, 医学部, 助手 (30250872)
MIYAZAKI Akihisa School of Medicine, Juntendo University, Associate Professor, 医学部, 助教授 (20200149)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | gastric ulcer / growth factor / cytokine / migration / differentiation / Helicobacter pylori / HSP / stress / 損傷修復 / 細胞分裂 / ヘリコバクターピロリ / 胃粘膜損傷 / 消化性潰瘍 / 細胞培養 / 線維芽細胞 / 血管内皮細胞 / インスリン様増殖因子 / 細胞外基質 |
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| Research Abstract |
It has been generally accepted that the epithelial-mesenchymal interaction plays an important role in gut would repair process. In this project, we investigated the detailed mechanism of action of several growth factors, cytokines, ECM, toxic agents, trace minerals and physical stress in gut would healing using in vivo and in vitro would healing model. As expected, each growth factor has its own target cells and some growth factors show their effects by paracrine and autocrine mechanism. Among these growth factors, insulin-like growth factor 1 played a key role in gastric wound healing in vivo and in vitro. In this mechanism zinc stimulated the production of insulin-like growth factor 1 from fibroblasts and endothelial cells and induced insulin-like growth factor 1 affected to gastric epithelial cell migration and proliferation. In another series of experiments, we showed that heat shock protein 72 has cytoprotective effect in the stomach and pre-induction of heat shock protein 72 prevented gastric mucosal damage in the several experimental model with rats. In the experiment using strain stress in vitro, heat shock protein 72 was found in decreased significantly in the gastric epithelial cells and strain stress also inhibited gastric epithelial migration and proliferation resulting in the delay of wound healing. In the clinical situation, we found the inhibition of the heat shock protein expression in the Helicobacter pylori infected gastric mucosa. Therefore heat shock protein as well as growth factors may play an important role in the integrity of gastric mucosal damage and wound healing.
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