1998 Fiscal Year Final Research Report Summary
Mechanism for cellular cholesterol remoral mediated by an apolipoprotein receptor(s)
| Project/Area Number |
09470035
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | Nagoya City University |
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Principal Investigator |
YOKOYAMA Sinji Nagoya City University, Medical School, professor, 医学部, 教授 (10142192)
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| Co-Investigator(Kenkyū-buntansha) |
TSUJITA Maki Nagoya City University, Medical School, research associate, 医学部, 助手 (10253262)
ABE-DOHMAE Sumiko Nagoya City University, Medical School, assistant professor, 医学部, 講師 (70227700)
ITO Jinichi Nagoya City University, Medical School, assistant professor, 医学部, 講師 (60167260)
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| Project Period (FY) |
1997 – 1998
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| Keywords | Cholesterol / HDL / Apolipoprotein / Cell / Signal Transduction |
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| Research Abstract |
Two independent mechanisms are known for cellular cholesterol removal ; physicochemical diffusion and apolipoprotein-cell interaction that causes HDL neogenesis. This research project focused on the latter pathway to achieve the results as follows. 1) First year. In mouse peritoneal macrophages, PKC inhibitors suppressed the incorporation of cell cholesterol into the HDL generated with apolipoproteins though apolipoprotein binding to the cell and generation of HDL itself are uninfluenced, showing that this is due to inhibition of specific intracellular cholesterol trafficking. Mouse monocytic leukemia cell line cells RAW264 do not interact with apolipoprotein for HDL generation until cAMP induces the expression of the interaction site. 2) Second year. The induction of the interaction site by cAMP in RAW264 was suppressed by inhibition of transcription, protein synthesis and protein transport, showing the involvement of membrane protein in the interaction site. Human monocytic leukemia cell line cells THP1 generate cholesterol-poor HDL with apolipoprotein, and differentiation by PMA results in the specific increase of cholesterol content in HDL.This cells line have therefore been shown to be a good model for induction of specific intracellular cholesterol trafficking.
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