Analysis of Pancreatic Acinar Cell Apoptosis During Acute Pancreatitis
| Project/Area Number |
10670495
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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 | Kyoto Prefectural University of Medicine |
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Principal Investigator |
KASHIMA Kei Kyoto Prefectural University of Medicine, 3rd Department of Internal Medicine, Professor, 医学部, 教授 (30079818)
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| Co-Investigator(Kenkyū-buntansha) |
KATAOKA Keisho Kyoto Prefectural University of Medicine, 3rd Department of Internal Medicine, Assistant Professor, 医学部, 講師 (70185792)
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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 |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1999: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | pancreatic acinar cell apoptosis / pancreatic duct ligation / Fas / glucocorticoid / 266-6 cells / RU486 / マウス膵管結紮モデル / Fas |
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| Research Abstract |
To clarify the role of acinar cell apoptosis in the pathogenesis of acute pancreatitis, we investigated the expression of Fas and Fas ligand in mice after pancreatic duct ligation (PDL). Acinar cell apoptosis induced after PDL was observed at the rate of 0% (H-342) and 0.1%(TUNEL), and 2.7%(H-342) and 1.8%(TUNEL) of acinar cells on days 1 and 3 after PDL, respectively. Fas and Fas ligand mRNAs were detected on days 1 and 3 after PDL. Immunohistochemistry revealed that Fas ligand was expressed in acinar cells on day 3 after PDL. PDL in mice synchronously induced the expression of apoptosis and Fas ligand in acinar cells. The present results suggest that acinar cell apoptosis induced after PDL may be mediated by the Fas-Fas ligand system.
Furthermore, to clarify the role of glucocorticoid in acinar cell apoptosis, we investigated the effect of glucocorticoid receptor antagonist (RU486) in mouse pancreatic acinar cell line (266-6 cells). The number of 266-6 cells reduced to 40% of control group after 24-h RU486 (100μm) treatment. FACS methods revealed that the number of apoptotic 266-6 cells significantly increased after 9-h RU486(50μm) treatment. The present results suggest that the depletion of glucocorticoid induced apoptosis of 266-6 cells and glucocorticoid may protect the pancreatic acinar cells from apoptosis.
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Report
(3 results)
Research Products
(24 results)
