| Project/Area Number |
09670514
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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 | The University of Tokyo |
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Principal Investigator |
OHNO Akihiko UNIV. OF. TOKYO, FAC. OF MEDICINE, INSTRUCTOR, 医学部・附属病院, 助手 (30223902)
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| Co-Investigator(Kenkyū-buntansha) |
TOMIYA Tomoaki UNIV. OF. TOKYO, FAC. OF MEDICINE, INSTRUCTOR, 医学部・附属病院, 助手 (90227637)
IKEDA Hitoshi UNIV. OF. TOKYO, FAC. OF MEDICINE, INSTRUCTOR, 医学部・附属病院, 助手 (80202422)
MOCHIDA Sotoshi SAITAMA MEDICAL SCHOOL, DEP. OF INTERNAL MEDICINE, ASSISTANT PROFESSOR, 医学部, 講師 (20219968)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1998: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1997: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | HEPATOCYTE / ADHESION MOLECULE / ICAM-1 / LIVER INJURY / MACROPHAGE ACTIVATION |
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| Research Abstract |
To clarify the expression mechanism of adhesion molecules and its significance for liver injury, the expression of intercellular adhesion molecule-1 (ICAM-1) as well as lymphocyte function-associated antigen-1 (LFA-1) on hepatocytes and hepatic sinusoidal cells was investigated in rats. As for the relationship of these expressions to the activation of hepatic macrophages, ICAM-1 expression in endothelial cells can be associated with the stimulatory stage and the excitation extent of macrophages. LFA-1 expression in hepatic macrophages may depend on their activity in phagocytosis and/or excitation. Because these expressions were decreased by suppression of macrophage activity, it was suggested that regulation of the expression was closely related to the activation of hepatic macrophages.
In carbon tetrachloride-intoxicated or perfused liver, ICAM-1 protein was detected immunohistochemically on plasma membrane in degenerative hepatocytes. But ICAM-1 mRNA was not shown in these cells by in situ hybridization. These results suggested that ICAM-1 expression in degenerative hepatocytes might not result from de novo synthesis, but from dissociation of cell-to-cell contact.
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