1999 Fiscal Year Final Research Report Summary
Biological modulation of the epithelial-mesenchymal interaction in gut wound repair process.
| 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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| Keywords | gastric ulcer / growth factor / cytokine / migration / differentiation / Helicobacter pylori / HSP / stress |
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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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[Publications] S Watanabe, XE Wang, M Hirose, T Kivilioto, T Osada, H Miwa, H Oide, T Kitamura, T Yoneta, K Seto, N Sato: "Insulin like growth factor-1 plays a Role in gastric would healing : Evidence using a zinc derivative, polaprezinc, and an in vitro rabbit wound repair model."Aliment Pharmacol Ther. 12. 1131-1138 (1998)
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「研究成果報告書概要(欧文)」より
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[Publications] N Sato, S Watanabe, Xe Wang, T Osada, H Tanaka, T Itatsu, R Miyata, K Watanabe, K Sato, M Nakajima, S Yamashina, H Miwa: "A histamine H2 Receptor antagonist, FRG-8813, prevented the delay of wound repair induced by hydrogen peroxide in a rabbit gastric epithelial cell system."J Gastoenterol Hepatol. 13. s209-s213 (1998)
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[Publications] T Itatsu, H Miwa, R Ohkura, R Iwazaki, H Oide, T Murai, M Nakajima, S Watanabe, S Hirai, M Otaka, N Sato: "Primary gastric T-cell lymphoma accompanied by HTLV-1, HBV and H. pylori infection."Dig Dis Sci. 44. 1823-1836 (1999)
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「研究成果報告書概要(欧文)」より
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