| Project/Area Number |
11670475
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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 | GUNMA UNIVERSITY |
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Principal Investigator |
TAKAGI Hitoshi GUNMA UNIVERSITY SCHOOL OF MEDICINE, TEACHING ASSOCIATE, 医学部, 助手 (20251093)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2000: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1999: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | MUCOSA / TRANSGENIC / TGFα / HGF / VEGF / Ulcer / EGF-R |
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| Research Abstract |
Various growth factors are involved at recovery stage of gastric mucosal lesion such as gastric ulcer. In the present study, we focused on the hepatocyte growth factor (HGF) and transforming growth factor alpha (TGFa). Transgenic mice of HGF and TGFa whose promoter is under the control of metallothionein and the transgene is widely expressed in the epithelium including gastric mucosa.
First, the expression of HGF transgene was universally expressed in forestomach, body and antrum by northern blot. Mice were anesthetized by Nembutal and opened the abdomen. Metal probe was cooled by liquid nitrogen and attached to the serosal membrane. This method is established as a cooling method for experimental gastric ulcer but the size of experimental ulcer was not stable in this experiment. The ulcers in transgenic and non-transgenic mice were not different in size but the recovery phase were accelerated in HGF mice under the microscopic examination. Vascular endothelial growth factor was more expressed around the ulcer formation in HGF mouse than in nontransgenic mice. This might implicate the involvement of angiogenic collaboration between HGF and VEGF in the recovery phase of gastric ulcer.
Furthermore, TGFa mice ingested 150mM hydrogen chloride containing 60% ethanol by nasal to gastric intubation method. The mice were induced acute gastric mucosal lesions but there were no differences between TGFa mice and control mice in ulcer formation. The recovery tended to be accelerated in TGFa transgenic mice compared with non-transgenic mice. Additional study including time course is needed to clarify the difference of cell proliferation in transgenic mice and control.
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