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Motohiro Takeya
Department Kumamoto Health Science University Department of Medical Technology, Faculty of Health Science Position Professor |
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| Research Period | 2004～2005 |
| Research Topic | Elucidation of the mechanisms for intracellular accumulation of cholesterol ester and its application to therapies. |
| Research Type | KAKENHI Research |
| Consignor | Ministry of Education, Culture, Sports, Science and Technology |
| Research Program Type | Grants-in-Aid for Scientific Research(基盤研究(C)),基盤研究(C) |
| KAKENHI Grant No. | 16590895 |
| Representative Person | Akira MIYAZAKI |
| Collaborative Researcher | Shigeki HONGO, Motohiro TAKEYA, Takuya WATANABE |
| Details | Acyl-coenzyme A : cholesterol acyltransferase-1 (ACAT-1) converts intracellular free cholesterol into cholesterol ester for storage in lipid droplets and plays an important role in the formation of macrophage-derived foam cells in atherosclerotic lesions. Serotonin (5-HT), a potentvasoconstrictor that is released from activated platelets, increases uptake of oxidized low-density lipoprotein (LDL) by macrophages, leading to foam cell formation, and contributes to the development of atherosclerotic plaque. However, it is not yet known whether 5-HT affects ACAT-1 expression in human monocyte-macrophages as the molecular mechanism of 5-HT-induced foam cell formation. We examined the effects of 5-HT on ACAT-1 expression during differentiation of cultured human monocytes into macrophages. Expression of ACAT-1 protein but not 5-HT_<2A>receptor increased in a time-dependent manner. 5-HT increased ACAT activity in a concentration-dependent manner after seven days in primary monocyte culture. Immunoblotting analysis showed that 5-HT at 10μM increased ACAT-1 protein expression level by two-fold, and this effect was abolished completely by a 5-HT_<2A>receptor antagonist (sarpogrelate), Nor |
| Permalink URL | https://kaken.nii.ac.jp/d/p/16590895.ja.html |