MISC

2006年1月

Cell surface-expressed moesin-like HDL/apoA-I binding protein promotes cholesterol efflux from human macrophages

JOURNAL OF LIPID RESEARCH
  • A Matsuyama
  • ,
  • N Sakai
  • ,
  • H Hiraoka
  • ,
  • K Hirano
  • ,
  • S Yamashita

47
1
開始ページ
78
終了ページ
86
記述言語
英語
掲載種別
DOI
10.1194/jlr.M500425-JLR200
出版者・発行元
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC

HDL and its major component, apolipoprotein A-I (apoA-I), play a central role in reverse cholesterol transport. We recently reported the involvement of a glycosylphosphatidylinositol anchor (GPI anchor) in the binding of HDL and apoA-I on human macrophages, and purified an 80 kDa HDL/apoA-I binding protein. In the present study, we characterized the GPI-anchored HDL/apoA-I binding protein from macrophages. The HDL/apoA-I binding protein was purified from macrophages and digested with endopeptidase, and the resultant fragments were sequenced. Cholesterol efflux, flow cytometry, immunoblotting, and immunohistochemical analyses were performed to characterize the HDL/apoA-I binding protein. Two parts of seven amino acid sequences completely matched those of moesin. Flow cytometry, immunoblotting, and immunohistochemistry using anti-moesin antibody showed that the HDL/apoA-I binding protein was N-glycosylated and expressed on the cell surface. It was termed moesin-like protein. Treatment of macrophages with anti-moesin antibody blocked the binding of HDL/apoA-I and suppressed cholesterol efflux. The moesin-like protein was exclusively expressed on macrophages and was upregulated by cholesterol loading and cell differentiation. Our results indicate that the moesin-like HDL/apoA-I binding protein is specifically expressed on the surface of human macrophages and promotes cholesterol efflux from macrophages.

リンク情報
DOI
https://doi.org/10.1194/jlr.M500425-JLR200
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000234291300008&DestApp=WOS_CPL
ID情報
  • DOI : 10.1194/jlr.M500425-JLR200
  • ISSN : 0022-2275
  • eISSN : 1539-7262
  • Web of Science ID : WOS:000234291300008

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