1987 Fiscal Year Final Research Report Summary
Rele of the interaction between arterial smooth muscle cellsand endothelial cell or macrophages in foam cell formation.
| Project/Area Number |
61570300
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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 |
内科学一般
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| Research Institution | The 2nd Department of Internal Meicine, School of Medicine, Chiba University |
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Principal Investigator |
SAITO Yasushi The 2nd Department of Internal Medicine, Chiba University, 内科学第二講座, 講師 (50101358)
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| Co-Investigator(Kenkyū-buntansha) |
MORISAKI Nobuhiro The 2nd Department of Internal Medicine, Chiba University, 内科学第二講座, 助手 (40174411)
SHIRAI Kohji The 2nd Department of Internal Medicine, Chiba University, 内科学第二講座, 助手 (00150269)
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| Project Period (FY) |
1986 – 1987
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| Keywords | Cell to cell interaction / Intimal smooth muscle cell / Medial smooth muscle cell / Macrophage / Endothelial cell, |
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| Research Abstract |
1 Interaction between macrophages and smooth muscle cells (SMC):
<beta>-VLDL ([^3H]cholesterol ester labeled ) was incubated with macrophages and the conditioned medium was added to the smooth muscle cells. The incorporated radioactivities into SMC were increased by incubation with <beta>-VLDL containing medium conditioned with macrophages, comparing to those conditioned without macrophages. The increase in incorporated radioactivities into SMC was also obseryed with IDL containing medium conditioned with macrophage. Conditioning of <beta>-VLDL or IDL with macrophages produced lipid-protein particles (d = 1.19, <beta>-mobility). These results suggest that macrophage-SMC interaction might promote the foam cell formation with <beta>-VLDL.or IDL.
2. Interaction between endothelial cells and smooth muscle cells:
Medial SMC was cultured from aortic media and intimal SMC was cultured from canulated aortic intima. The intiaml SMC proliferation increased comparing to that of medial SMC. By co-culturing of these SMC with endothelial cells, the proliferation of medial SMC was inhibited, but proliferation of intimal SMC was bit inhibited. These results suggest that SMC proliferation was regulated by endothelial cells, and loss of endothelial cell may promote proliferation of medial SMC.
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[Publications] Kanzaki, T., Ishikawa, Y., Morisaki, N., Shirai, K., Saito, Y., and Yoshida, S.: "Abnormal Metabolism of Polyunsaturated Fatty Acids and Phospholipids in Diabetic Glomeruli." Lipids. 22. 704-710 (1987)
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「研究成果報告書概要(欧文)」より
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[Publications] Murano,S., Shirai, K., Saito, Y., Yoshida, S., Othta, Y., Tsuchida, H., Yamamoto, S., Asano, G., Chen, C. H., and Albers J.J.: "Impaired Intermediate-Density Lipoprotein Triglyceride Hydrolysis in Familial Lecithin; Cholesterol Acyltransferase (LCAT) Deficiency." Scand. J. Clin. Lab. Invest.47. 775-783 (1987)
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「研究成果報告書概要(欧文)」より
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