Changes in plasma membrane properties and phosphatidylcholine subspecies of insect Sf9 cells due to expression of scavenger receptor class B, type I, and CD36.
In mammalian cells scavenger receptor class B, type I (SR-BI), mediates the selective uptake of high density lipoprotein (HDL) cholesteryl ester into hepatic and steroidogenic cells. In addition, SR-BI has a variety of effects on plasma membrane properties including stimulation of the bidirectional flux of free cholesterol (FC) between cells and HDL and changes in the organization of plasma membrane FC as indicated by increased susceptibility to exogenous cholesterol oxidase. Recent studies in SR-BI-deficient mice and in SR-BI-expressing Sf9 insect cells showed that SR-BI has significant effects on plasma membrane ultrastructure. The present study was designed to test the range of SR-BI effects in Sf9 insect cells that typically have very low cholesterol content and a different phospholipid profile compared with mammalian cells. The results showed that, as in mammalian cells, SR-BI expression increased HDL cholesteryl ester selective uptake, cellular cholesterol mass, FC efflux to HDL, and the sensitivity of membrane FC to cholesterol oxidase. These activities were diminished or absent upon expression of the related scavenger receptor CD36. Thus, SR-BI has fundamental effects on cholesterol flux and membrane properties that occur in cells of evolutionarily divergent origins. Profiling of phospholipid species by electrospray ionization mass spectrometry showed that scavenger receptor expression led to the accumulation of phosphatidylcholine species with longer mono- or polyunsaturated acyl chains. These changes would be expected to decrease phosphatidylcholine/cholesterol interactions and thereby enhance cholesterol desorption from the membrane. Scavenger receptor-mediated changes in membrane phosphatidylcholine may contribute to the increased flux of cholesterol and other lipids elicited by these receptors.
Department of Pharmacological Sciences, University Medical Center, State University of New York, Stony Brook, New York 11794-8651, USA. parathath@phharm.sunysb.edu
Saj
S
Parathath
Margery A
MA
Connelly
Robert A
RA
Rieger
Seth M
SM
Klein
Nada A
NA
Abumrad
Margarita
M
De La Llera-Moya
Charles R
CR
Iden
George H
GH
Rothblat
David L
DL
Williams
D000818:Animals; D018955:CD36 Antigens / Q000235:genetics / Q000502:physiology*; D002460:Cell Line; D002462:Cell Membrane / Q000737:chemistry / Q000378:metabolism*; D002784:Cholesterol / Q000378:metabolism; D002788:Cholesterol Esters / Q000378:metabolism; D002789:Cholesterol Oxidase / Q000378:metabolism; D007313:Insecta; D008075:Lipoproteins, HDL / Q000378:metabolism; D013058:Mass Spectrometry; D051379:Mice; D010713:Phosphatidylcholines / Q000032:analysis* / Q000378:metabolism; D010743:Phospholipids / Q000032:analysis; D051381:Rats; D011971:Receptors, Immunologic / Q000235:genetics / Q000502:physiology*; D051116:Receptors, Scavenger; D051122:Scavenger Receptors, Class B; D014162:Transfection
D018955:CD36 Antigens; D002788:Cholesterol Esters; C059714:HDL cholesteryl ester; D008075:Lipoproteins, HDL; D010713:Phosphatidylcholines; D010743:Phospholipids; D011971:Receptors, Immunologic; D051116:Receptors, Scavenger; C495125:Scarb1 protein, rat; D051122:Scavenger Receptors, Class B; D002784:Cholesterol; D002789:Cholesterol Oxidase