Quantitation of pre beta-HDL-dependent and nonspecific components of the total efflux of cellular cholesterol and phospholipid.
Both receptor-mediated and diffusional processes have been proposed as mechanisms for the efflux of cellular cholesterol to plasma. The depletion of a minor high-density lipoprotein subfraction (pre beta-1-HDL) from plasma by incubation was associated with a proportional reduction in up to 58% of cholesterol and lecithin efflux from cultured fibroblasts. Pre beta-HDL-dependent efflux was blocked by protease pretreatment of the cells, while residual ("nonspecific") efflux was protease-insensitive. The whole of cholesterol efflux from blood erythrocytes was both pre beta-1-HDL-and protease-independent. These data suggest that two distinct pathways contribute to total efflux from fibroblast monolayers; one of these is directly proportional to plasma pre beta-1-HDL concentration and may involve a cell-surface protein.
Cardiovascular Research Institute, University of California, San Francisco 94143.
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M
Kawano
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Miida
C J
CJ
Fielding
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PE
Fielding
D002478:Cells, Cultured; D002784:Cholesterol / Q000097:blood*; D002794:Choline / Q000378:metabolism; D010450:Endopeptidases / Q000494:pharmacology; D004912:Erythrocytes / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism; D006801:Humans; D007700:Kinetics; D008075:Lipoproteins, HDL / Q000097:blood*; D010743:Phospholipids / Q000097:blood*
D008075:Lipoproteins, HDL; D010743:Phospholipids; D002784:Cholesterol; D010450:Endopeptidases; D002794:Choline