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Journal of Lipid Research, Vol 38, 1807-1821, Copyright © 1997 by Lipid Research, Inc.
AJ Mendez
It is becoming increasingly accepted that removal of cellular cholesterol
occurs by at least two pathways, one involving the well- described aqueous
diffusion mechanism and another promoted by lipid- free apolipoproteins. We
compared the contribution of apolipoprotein- dependent and -independent
pathways, taking into consideration the influence of cellular metabolism,
on cholesterol efflux promoted by different extracellular acceptor types.
The acceptors used were assumed to participate in only passive efflux by
lipid-dependent mechanisms (phospholipid vesicles and trypsin-modified high
density lipoproteins) or to stimulate efflux by apolipoprotein-dependent
pathways (purified apolipoprotein A-I and high density lipoproteins).
Apolipoprotein- mediated cholesterol efflux was only apparent in
growth-arrested or cholesterol-enriched cells and required metabolic
energy. In contrast, cholesterol efflux by apolipoprotein-depleted
acceptors did not depend on cell growth state, cholesterol enrichment, or
metabolic energy. Apolipoprotein-mediated efflux was not observed at
temperatures below 22 degrees C, while apolipoprotein-independent efflux
was only reduced by 50% at 4 degrees C compared with incubations at 37
degrees C. Additionally, apolipoproteins promoted a more rapid and larger
decrease in intracellular cholesteryl esters when measured by changes in
cholesteryl ester radioactivity, mass, or the pool of cholesterol available
for esterification by acyl coenzyme A:cholesterol acyltransferase. Efflux
of excess cellular cholesterol by an apolipoprotein-dependent pathway
appears to involve specific cellular events consistent with the properties
of an active transport pathway and distinguishable from cholesterol efflux
by apolipoprotein-depleted acceptors through passive mechanisms.
ARTICLES
Cholesterol efflux mediated by apolipoproteins is an active cellular process distinct from efflux mediated by passive diffusion
University of Miami School of Medicine, Diabetes Research Institute, Miami, FL 33101, USA.
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