| Project/Area Number |
01570407
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Department of Internal Medicine (Section 4), Sapporo Medical College |
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Principal Investigator |
KOHGO Yutaka Department of Internal Medicine (Section 4), Sapporo Medical College Associate Professor, 医学部, 助教授 (10133183)
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| Co-Investigator(Kenkyū-buntansha) |
MOGI Yoshihiro Department of Internal Medicine (Section 4), Sapporo Medical College Assistant P, 医学部, 講師 (30190953)
NIITSU Yoshiro Department of Internal Medicine (Section 4), Sapporo Medical College Professor, 医学部, 教授 (10045502)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1990: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1989: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Ethanol / Asialoglycoprotein receptor / Protein synthesis regulation / アシアロ糖蛋白白受容体 / アルコ-ル / 肝細胞膜 / HepG2細胞 / Northern blot / Western blot |
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| Research Abstract |
We studied the effect of ethanol on the expression of asialoglycoprotein receptor of a human hepatoma cell line, Hep G2 cells, which has been shown to maintain a large variety of normal hepatocyte functions. By ethanol treatment, the number of asialoglycoprotein receptors on the cell surface decreased to 60% of the control, with no change of binding affinity. The decrease of cell surface asialoglycoprotein receptors was parallel to that of total receptor number including surface and intracellular receptors. Internalization of asialoglycoprotein receptors was also diminlshed to 45% of control cells. Northern blot analysis by using a human asialoglycoprotein receptor oligonucleotide probe showed an increase of the specific asialoglycoprotein receptor mRNA in ethanol-treated cells. The amount of newly synthesized AGPR was decreased in ethanol-treated HeP G2 cells. This increase was reversible when cells were removed from ethanol. These results suggest that ethanol metabolite directly induce the decrease of asialoglycoprotein receptor in human hepatocytes at post translational level. The paradoxical increase of asialoglycoprotein receptor mRNA after ethanol treatment could be explained by the possible feed-back mechanism which controls asialoglycoprotein receptor gene transcription and/or impaired degradation of receptor mRNA.
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