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  • 标题:Homozygous disruption of Pctp modulates atherosclerosis in apolipoprotein E-deficient mice
  • 本地全文:下载
  • 作者:Wang, Wen-Jun ; Baez, Juan M. ; Maurer, Rie
  • 期刊名称:JLR Papers In Press
  • 印刷版ISSN:0022-2275
  • 电子版ISSN:1539-7262
  • 出版年度:2006
  • 卷号:47
  • 期号:11
  • 页码:2400-2407
  • DOI:10.1194/jlr.M600277-JLR200
  • 出版社:American Society for Biochemistry and Molecular Biology
  • 摘要:Phosphatidylcholine transfer protein (PC-TP) is a cytosolic phospholipid binding protein and a member of the steroidogenic acute regulatory-related transfer domain superfamily. Its tissue distribution includes liver and macrophages. PC-TP regulates hepatic lipid metabolism, and its absence in cholesterol-loaded macrophages is associated with reduced ATP binding cassette transporter A1-mediated lipid efflux and increased susceptibility to apoptosis induced by unesterified cholesterol. To explore a role for PC-TP in atherosclerosis, we prepared PC-TP-deficient/apolipoprotein E-deficient (Pctp–/–/Apoe–/–) mice and littermate Apoe–/– controls. At 16 weeks, atherosclerosis was increased in chow-fed male, but not female, Pctp–/–/Apoe–/– mice. This effect was associated with increases in plasma lipid concentrations. By contrast, no differences in atherosclerosis were observed between male or female Pctp–/–/Apoe–/– mice and Apoe–/– controls fed a Western-type diet for 16 weeks. At 24 weeks, atherosclerosis in chow-fed male Pctp–/–/Apoe–/– mice tended to be reduced in proportion to plasma cholesterol. The attenuation of atherosclerosis in female Pctp–/–/Apoe–/– mice fed chow or the Western-type diet for 24 weeks was not attributable to changes in plasma cholesterol or triglyceride concentrations. These findings suggest that PC-TP modulates the development of atherosclerosis, in part by regulating plasma lipid concentrations. Supplementary key words phosphatidylcholine transfer protein • steroidogenic acute regulatory-related transfer domain • cholesterol • triglycerides • aorta • macrophage Abbreviations: apoE, apolipoprotein E; PC-TP, phosphatidylcholine transfer protein; START, steroidogenic acute regulatory-related transfer
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