2002 Fiscal Year Final Research Report Summary
Expression and the role of fibroblast growth factor (FGF)-10 in chronic pancreatitis
| Project/Area Number |
13670571
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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 | Nippon Medical School |
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Principal Investigator |
ISHIWATA Toshiyuki Nippon Medical School, Medicine, Assistant Professor, 医学部, 講師 (90203041)
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| Co-Investigator(Kenkyū-buntansha) |
NAITO Zenya Nippon Medical School, Medicine, Associate Professor, 医学部, 助教授 (20237184)
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| Project Period (FY) |
2001 – 2002
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| Keywords | fibroblast growth factor (FGF)-10 / pancreatitis / FGF-7 / Keratinocyte growth factor receptor / Immunohistochemistry / Western blot analysis |
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| Research Abstract |
The regenerative process in acute and chronic pancreatitis is characterized by acinar and ductal cell proliferation with synthesis and deposition of extracellular matrices. Various growth factors are closely related to the inflammatory process of pancreatitis. Fibroblast growth factor (FGF)-10 and FGF-7, also known as keratinocyte growth factor (KGF), are members of the FGF family and show high structural homology as well as similar biological characteristics. Both of them are synthesized by mesenchymal cells and stimulate epithelial cells via KGF receptor (KGFR). We examined the localization of FGF-10, FGF-7 and KGFR in pancreatic tissues in an L-arginine-induced rat pancreatitis model. FGF-10 immunoreactivity was not detected in normal rat pancreas, but it was localized in vascular smooth muscle cells in L-arginine-induced acute pancreatitis. FGF-7 expression was limited in the alpha cells of islets in normal and L-arginine-treated pancreata. We then tested with rabbit polyclonal antibody specific for KGFR, and found the KGFR immunoreactivity was localized in centroacinar, islet and ductal cells in normal pancreata and strongly localized in regenerative acinar and islet cells in the pancreatitic tissues. In human chronic pancreatitic tissues from autopsy cases, KGFR was prominently localized in ductal, acinar and islet cells in regenerative regions. These findings suggest that FGF-10 and FGF-7 contribute to the reaenerative process of acute and chronic pancreatitis via KGFR.
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