論文

査読有り
2004年9月

Early-phase redistribution of the cation-independent mannose 6-phosphate receptor by U18666A treatment in HeLa cells

CELL AND TISSUE RESEARCH
  • Y Tomiyama
  • ,
  • S Waguri
  • ,
  • S Kanamori
  • ,
  • S Kametaka
  • ,
  • M Wakasugi
  • ,
  • M Shibata
  • ,
  • S Ebisu
  • ,
  • Y Uchiyama

317
3
開始ページ
253
終了ページ
264
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1007/s00441-004-0941-3
出版者・発行元
SPRINGER

It has been shown that the treatment with 3beta-[2-(diethylamino)ethoxy] androst-5-en-17-one (U18666A) causes the accumulation of cholesterol and the cation-independent mannose 6-phosphate receptor (CIMPR) in late endosomal/lysosomal compartments in BHK cells. The present study reports on a study of the effect of U18666A on CIMPR distribution in more detail in HeLa cells. When cells were treated with U18666A for 20 h, the intense perinuclear signal for CIMPR corresponding to the trans-Golgi network (TGN) disappeared and lamp1-negative punctate signals, scattered in the perinuclear region were detected. CIMPR then began to accumulate in lamp1-positive compartments 48 h after addition of the drug. Double immunofluorescence microscopy showed that U18666A-induced mannose 6-phosphate receptor-containing compartments (U-MPRCs), which were formed in the early phase of the redistribution, contained no marker for the TGN, late endosomes or lysosomes. Approximately half of the structures contained transferrin that had been internalized for 20 min, and cathepsin D, the majority of which appeared to be its precursor form. Immunoelectron-microscopic analysis revealed that U-MPRCs are composed of multivesicular bodies, irregularly shaped structures, and vesicular structures adjacent to the multivesicular bodies. These results suggest that U18666A treatment primarily suppresses the CIMPR transport pathways to late endosomes and from transferrin-containing endosomes, both of which may be dependent on cholesterol function.

リンク情報
DOI
https://doi.org/10.1007/s00441-004-0941-3
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/15322907
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000223464500004&DestApp=WOS_CPL
ID情報
  • DOI : 10.1007/s00441-004-0941-3
  • ISSN : 0302-766X
  • PubMed ID : 15322907
  • Web of Science ID : WOS:000223464500004

エクスポート
BibTeX RIS