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J. Biol. Chem., Vol. 275, Issue 47, 36596-36604, November 24, 2000
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From the The role of high density lipoprotein (HDL)
phospholipid in scavenger receptor BI (SR-BI)-mediated free cholesterol
flux was examined by manipulating HDL3
phosphatidylcholine and sphingomyelin content. Both phosphatidylcholine
and sphingomyelin enrichment of HDL enhanced the net efflux of
cholesterol from SR-BI-expressing COS-7 cells but by two different
mechanisms. Phosphatidylcholine enrichment of HDL increased efflux,
whereas sphingomyelin enrichment decreased influx of HDL cholesterol.
Although similar trends were observed in control (vector-transfected)
COS-7 cells, SR-BI overexpression amplified the effects of
phosphatidylcholine and sphingomyelin enrichment of HDL 25- and
2.8-fold, respectively. By using both phosphatidylcholine-enriched and
phospholipase A2-treated HDL to obtain HDL with a graded
phosphatidylcholine content, we showed that SR-BI-mediated cholesterol
efflux was highly correlated (r2 = 0.985) with
HDL phosphatidylcholine content. The effects of varying HDL
phospholipid composition on SR-BI-mediated free cholesterol flux were
not correlated with changes in either the Kd or
Bmax values for high affinity binding to SR-BI.
We conclude that SR-BI-mediated free cholesterol flux is highly
sensitive to HDL phospholipid composition. Thus, factors that regulate
cellular SR-BI expression and the local modification of HDL
phospholipid composition will have a large impact on reverse
cholesterol transport.
High Density Lipoprotein Phospholipid Composition Is a Major
Determinant of the Bi-directional Flux and Net Movement of Cellular
Free Cholesterol Mediated by Scavenger Receptor BI*
,,,
Division of Gastroenterology and
Nutrition, Department of Pediatrics, The Children's Hospital of
Philadelphia, Philadelphia, Pennsylvania 19104 and the
§ Department of Pharmacological Sciences, University Medical
Center, State University of New York,
Stony Brook, New York 11794
*
This work was supported by National Institutes of Health
Grants HL22633, HL58012, and HL63768 and additional funding from Pfizer
Central Research.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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