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Journal of Lipid Research, Vol 36, 544-551, Copyright © 1995 by Lipid Research, Inc.
T Mazzone, M Krishna and Y Lange
Macrophage foam cells must accommodate continuing fluxes of free
cholesterol in spite of a greatly expanded store of cholesteryl ester.
Though endogenous free cholesterol synthesis is suppressed, free
cholesterol continues to enter the cell via endocytosis of
oxidized/modified lipoproteins. It has been shown previously that this free
cholesterol is released into the lysosomal compartment and rapidly
transported to the plasma membrane prior to its esterification. A
substantial amount of free cholesterol is also presented via the continuous
hydrolysis of cholesteryl ester during the cholesteryl ester cycle. We
addressed the question of whether the intracellular free cholesterol
derived from the hydrolysis of cholesteryl ester formed a protected pool
for rapid re-esterification. Incubation of macrophage foam cells with
cyclic AMP to enhance cholesteryl ester hydrolysis, and with S58035 to
inhibit acyl-CoA:cholesterol acyltransferase (ACAT) activity, led to
conversion of cellular cholesteryl ester to free cholesterol and transport
of this free cholesterol to the plasma membrane. Addition of progesterone,
previously demonstrated to be an inhibitor of free cholesterol transport in
other cell types, also led to conversion of cholesteryl ester to free
cholesterol even though progesterone was only a weak inhibitor of ACAT
activity. Free cholesterol in the plasma membrane was an important source
of ACAT substrate to balance the constitutive hydrolysis of cholesteryl
ester in cholesterol-loaded macrophages. Treatment of cells with
progesterone, however, prevented free cholesterol derived from cholesteryl
ester hydrolysis from moving to the plasma membrane. The sequestration of
free cholesterol by progesterone could be reversed by incubation with human
HDL3.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Progesterone blocks intracellular translocation of free cholesterol derived from cholesteryl ester in macrophages
Department of Medicine, Rush Medical College, Chicago, IL 60612, USA.
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