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LOX-1 mediates lysophosphatidylcholine-induced oxidized LDL uptake in smooth muscle cells
被引:101
|作者:
Aoyama, T
Chen, MY
Fujiwara, H
Masaki, T
Sawamura, T
[1
]
机构:
[1] Natl Cardiovasc Ctr, Res Inst, Dept Biosci, Osaka 5658565, Japan
[2] Gifu Univ, Sch Med, Dept Internal Med 2, Gifu, Japan
[3] Osaka Univ, Grad Sch Pharmaceut Sci, Dept Mol Pathophysiol, Osaka, Japan
关键词:
lectin-like oxidized low-density lipoprotein receptor;
oxidized LDL;
vascular smooth muscle cell;
lysophosphatidylcholine;
atherosclerosis;
D O I:
10.1016/S0014-5793(00)01154-6
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
A novel receptor for oxidized low-density lipoprotein (OxLDL), lectin-like OxLDL receptor (LOX-1), was cloned from endothelial cells, Since OxLDL is taken up by vascular smooth muscle cells (VSMC) in atheroma, we analyzed the inducible expression of LOX-1 in VSMC in the present study. Incubation of cultured bovine VSMC with lysophosphatidylcholine (LPC), an atherogenic component of OxLDL, increased the level of mRNA for LOX-1 in a dose- and time-dependent manner. Since LPC did not significantly change the half-life of LOX-1 mRNA, the induction seemed to occur at the transcriptional level, The induction accompanied an increase in the protein level of LOX-1 and activity of OxLDL uptake. Blocking antibody against LOX-1 significantly suppressed the enhanced uptake of OxLDL, Thus, LOX-1 is a major receptor for OxLDL in VSMC as in endothelial cells. The enhanced expression of LOX-1 by LPC suggests that OxLDL and LPC would progressively change the function of VSMC and accelerate atherogenesis in vivo. (C) 2000 Federation of European Biochemical Societies.
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页码:217 / 220
页数:4
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