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Journal of Lipid Research, Vol. 42, 1740-1751, November 2001
Copyright © 2001 by Lipid Research, Inc.

Lipoprotein lipase mediates an increase in selective uptake of HDL-associated cholesteryl esters by cells in culture independent of scavenger receptor BI

Correspondence to: Franz Rinninger, To whom correspondence should be addressed., Rinninger{at}uke.uni-hamburg.de (E-mail)

Scavenger receptor class B type I (SR-BI) mediates the selective uptake of HDL cholesteryl esters (CEs) by the liver. LPL promotes this selective lipid uptake independent of lipolysis. In this study, the role of SR-BI in the mechanism of this LPL-mediated increase in selective CE uptake was explored. Baby hamster kidney (BHK) cells were transfected with the SR-BI cDNA, and significant SR-BI expression could be detected in immunoblots, whereas no SR-BI was visualized in control cells. Y1-BS1 murine adrenocortical cells were cultured without or with adrenocorticotropic hormone, and cells with no detectable or with SR-BI were obtained. These cells incubated without or with LPL in medium containing ¹²⁵I/[³H]cholesteryl oleyl ether- labeled HDL₃; tetrahydrolipstatin inhibited the catalytic activity of LPL. In BHK and in Y1-BS1 cells without or with SR-BI expression, apparent HDL₃ selective CE uptake ([³H]CEt - ¹²⁵I) was detectable. Cellular SR-BI expression promoted HDL₃ selective CE uptake by 250–1,900%. In BHK or Y1-BS1 cells, LPL mediated an increase in apparent selective CE uptake. Quantitatively, this stimulating LPL effect was very similar in control cells and in cells with SR-BI expression. The uptake of radiolabeled HDL₃ was also investigated in human embryonal kidney 293 (HEK 293) cells that are an established SR-BI-deficient cell model. LPL stimulated [³H]cholesteryl oleyl ether uptake from labeled HDL₃ by HEK 293 cells substantially, showing that LPL can induce selective CE uptake from HDL₃ independent of SR-BI. To explore the role of cell surface proteoglycans on lipoprotein uptake, we induced proteoglycan deficiency by heparinase treatment. Proteoglycan deficiency decreased the LPL-mediated promotion of HDL₃ selective CE uptake.

In summary, evidence is presented that the stimulating effect of LPL on HDL₃ selective CE uptake is independent of SR-BI and lipolysis. However, cell surface proteoglycans are required for the LPL action on selective CE uptake. It is suggested that pathways distinct from SR-BI mediate selective CE uptake from HDL. — Rinninger, F., M. Brundert, I. Brosch, N. Donarski, R. M. Budzinski, and H. Greten. Lipoprotein lipase mediates an increase in selective uptake of HDL-associated cholesteryl esters by cells in culture independent of scavenger receptor BI. J. Lipid Res. 2001. 42: 1740–1751.

Supplementary key words: adrenal, atherosclerosis, BHK, HEK 293, liver, metabolism, Y1-BS1

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