Scavenger receptor BI and cholesterol trafficking

Current Opinion in Lipidology

Volumn 10, Issue 4, 1999, Pages 329-339

  Williams, David L ^a   Connelly, Margery A ^a   Temel, Ryan E ^a   Swarnakar, Snehasikta ^a   Phillips, Michael C ^b   De la Llera Moya, Margarita ^b   Rothblat, George H ^b  

^a STONY BROOK UNIVERSITY MEDICAL CENTER   (United States)

^b DREXEL UNIVERSITY COLLEGE OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

APOLIPOPROTEIN B; CHOLESTEROL; CHOLESTEROL ESTER; HIGH DENSITY LIPOPROTEIN; SCAVENGER RECEPTOR;

ATHEROSCLEROSIS; HUMAN; LIPOPROTEIN METABOLISM; LIVER; PRIORITY JOURNAL; REVIEW;

ANIMALS; ANTIGENS, CD36; APOLIPOPROTEINS; ARTERIOSCLEROSIS; CHOLESTEROL; CHOLESTEROL ESTERS; HUMANS; LIPOPROTEINS, HDL; MEMBRANE PROTEINS; RECEPTORS, IMMUNOLOGIC; RECEPTORS, LIPOPROTEIN; RECEPTORS, SCAVENGER; SCAVENGER RECEPTORS, CLASS B;

ANIMALIA;

EID: 0032822860     PISSN: 09579672     EISSN: None     Source Type: Journal    
DOI: 10.1097/00041433-199908000-00007     Document Type: Review

References (97)

1. Calvo D, Vega MA. Identification, primary structure, and distribution of CLA-1, a novel member of the CD36/LlMPII gene family. J Biol Chem 1993; 268:18929-18935.
2. Acton SL, Scherer PE, Lodish HF, Krieger M. Expression Cloning of SR-BI, a CD36-related class B scavenger receptor. J Biol Chem 1994; 269:21003-21009.
3. Acton S, Rigotti A, Landschulz KT, Xu S, Hobbs HH, Krieger M. Identification of scavenger receptor SR-BI as a high density lipoprotein receptor. Science 1998; 271:518-520.
4. Gwynne JT, Hess B. The role of high density lipoproteins in rat adrenal cholesterol metabolism and steroidogenesis. J Biol Chem 1980; 255:10875-10883.
5. Glass C, Pittman RC, Weinstein DB, Steinberg D. Dissociation of tissue uptake of cholesterol ester from that of apoprotein A-I of rat plasma high density lipoprotein: Selective delivery of cholesterol ester to liver, adrenal, and gonad. Proc Natl Acad Sci USA 1983; 80:5435-5439.
6. Pittman RC, Knecht TP, Rosenbaum MS, Taylor CA Jr, A nonendocytotic mechanism for the selective uptake of high density lipoprotein-associated cholesterol esters. J Biol Chem 1987; 262:2443-2450.
7. Azhar S, Tsai L, Reaven E. Uptake and utilization of lipoprotein cholesteryl esters by rat granulosa cells. Biochim Biophys Acta 1990; 1047:148-160.
8. Reaven E, Spicher M, Azhar S. Microvillar channels: a unique plasma membrane compartment for concentrating lipoproteins on the surface of rat adrenal cortical cells. J Lipid Res 1989; 30:1551-1580.
9. Reaven E, Chen Y-DI, Spicher M, Azhar S. Morphological evidence that high density lipoproteins are not internalized by steroid-producing cells during in situ organ perfusion. J Clin Invest 1984; 74:1384-1397.
10. Goldberg DI, Beltz WF, Pittman RC. Evaluation of pathways for the cellular uptake of high density lipoprotein cholesterol esters in rabbits. J Clin Invest 1991; 87:331-346.
11. Rinninger F, Pittman RC. Regulation of the selective uptake of high density lipoprotein-assocaited cholesteryl esters by human fibroblasts and Hep G2 hepatoma cells. J Lipid Res 1988; 29:1179-1194.
12. Rinninger F, Brundert M, Jackle S, Galle PR, Busch C, Izbicki JR, et al. Selective uptake of high-density lipoprotein-associated cholesteryl esters by human hepatocytes in primary culture. Hepatology 1994; 19:1100-1119.
13. Azhar S, Tsai L, Medicherla S, Chandrasekher Y, Gudice L, Reaven E. Human granulosa cells use high density lipoprotein cholesterol for steroidogenesis. J Clin Endocrinol Metab 1998; 83:983-991. This report shows that human luteinized granulosa cells take up HDL cholesteryl ester almost exclusively by the selective uptake pathway and efficiently use the cholesteryl ester for progestin production. The efficiency of HDL cholesteryl ester uptake was equivilant to the uptake of LDL cholesteryl ester which was taken up mostly by endocytosis (75%) but also by the selective uptake pathway (25%).
14. Reaven E, Boyles J, Spicher M, Azhar S. Evidence for surface entrapment of cholesterol-rich lipoproteins in luteinized ovary. Arteriosclerosis 1988; 8:298-309.
15. Reaven E, Chen Y-DI, Spicher M, Hwang S-F, Mondon CE, Azhar S. Uptake of few density lipoproteins by rat tissues-special emphasis on the luteinized ovary. J Clin Invest 1986; 77:1971-1984.
16. Brissette L, Falstrault L. Analysts of the selective uptake of the cholesteryl ester of human intermediate density lipoproteins by HepG2 cells. Biochim Biophys Acta 1996; 1213:5-13.
17. Brissette L, Charest M-C, Falstrault L. Selective uptake of cholesteryl esters of low density lipoproteins is mediated by the lipoprotein binding site in HepG2 cells and is followed by the hydrolysis of cholesteryl esters. Biochem J 1996; 318:841-847.
18. Rinninger F, Brundert M, Jackle S, Kaiser T, Greter H. Selective uptake of low-density lipoprotein-associated cholesteryl esters by human fibroblasts, human HepG2 hepatoma cells and J774 macrophages in culture. Biochim Biophys Acta 1995; 1255:141-153.
19. Calvo D, Dopazo J, Vega MA. The CD36, CLA-1 (CD36L1), and LIMPII (CD36L2) gene family: cellular distribution, chromosomal location, and genetic evolution. Genomics 1995; 25:100-106.
20. Johnson MS, Svensson PA, Helou K, Billig H, Levan G, Carlsson LM, Carlsson B. Characterization and chromosomal localization of rat scavenger receptor class B type I, a high density lipoprotein receptor with a putative leucine zipper domain and peroxisomal targeting sequence. Endocrinology 1998; 139:72-80.
21. Mizutani T, Sonoda Y, Minegishi T, Wakabayashi K, Miyamoto K. Cloning, characterization, and cellular distribution of rat scavenger receptor class B type I (SRBI) in the ovary. Biochem Biophys Res Commun 1997; 234:499-505.
22. Rigotti A, Trigatti B, Babitt J, Penman M, Xu S, Krieger M. Scavenger Receptor Bl-a cell surface receptor for high density lipoprotein. Curr Opin Lipidol 1997; 8:181-188.
23. Webb NR, de Villiers WJ, Connell PM, De Beer FC, van der Westhuyzen DR. Alternative forms of the scavenger receptor BI (SR-BI). J Lipid Res 1997; 38:1490-1495.
24. Webb NR, Connell PM, Graf GA, Smart EJ, de Villiers WJS, DeBeer C, van der Westhuyzen D. SR-BII, an isoform of the scavenger receptor BI containing an alternate cytoplasmic tail, mediates lipid transfer between high density lipoprotein and cells. J Biol Chem 1998; 273:15241-15248. SR-BII is shown to be active in the selective uptake of HDL cholesteryl ester and to reduce HDL cholesterol levels after adenovirus-mediated hepatic expression.
25. Babitt J, Trigatti B, Rigotti A, et al. Murine SR-BI, a high density lipoprotein receptor that mediates selective lipid uptake, is N-glycosylated and fatty acylated and colocalizes with plasma membrane caveolae. J Biol Chem 1997; 272:13242-13249.
26. Murao K, Terpstra V, Green SR, Kondratenko N, Steinberg D, Quehenberger O. Characterization of CLA-1, a human homologue of rodent scavenger receptor BI, as a receptor for high density lipoprotein and apoptotic thymocytes. J Biol Chem 1997; 272:17551-17557.
27. Rigotti A, Acton S, Krieger M. The class B scavenger receptors SR-B1 and CD36 are receptors for anionic phospholipids. J Biol Chem 1995; 270:16221-16224.
28. Cao G, Garcia CK, Wyne KL, Schultz PA, Parker KL, Hobbs HH. Structure and localization of the human gene encoding SR-Bl/CLA-1. Evidence for transcriptional control by steroidogenic Factor 1 J Biol Chem 1997; 272:33068-33076.
29. Rigotti A, Edelman ER, Seifert P, et al. Regulation by adrenocorticotropic hormone of the in vivo expression of scavenger receptor class B type I (SR-B1), a high density lipoprotein receptor, in steroidogenic cells of the murine adrenal gland. J Biol Chem 1996; 271:33545-33549.
30. Landschulz KT, Pathak RK, Rigotti A, Krieger M, Hobbs HH. Regulation of scavenger receptor, class B, type I, a high density lipoprotein receptor, in liver and steroidogenic tissues of the rat. J Clin invest 1996; 98:984-995.
31. Temel RE, Trigatti B, DeMattos RB, Azhar S, Krieger M, Williams DL. Scavenger receptor B, type I (SR-BI) is the major route for the delivery of high density lipoprotein cholesterol to the steroidogenic pathway in cultured mouse adrenocortical cells. Proc Natl Acad SciUSA 1997; 94:13600-13605. Antibodies to the extracellular domain of SR-BI is shown to block the cell surface binding of HDL, the selective uptake of HDL CE and the utilization of HDL CE for steroid production in adrenocortical cells. These data demonstrate the function of SR-BI as the receptor responsible for most of the HDL CE selective uptake in cultured cells.
32. Rigotti A, Trigatti BL, Penman M, Rayburn H, Herz I, Krieger M. A targeted mutation in the murine gene encoding the high density lipoprotein (HDL) receptor scavenger receptor class B type I reveals its key role in HDL metabolism. Proc Natl Acad SciUSA 1997; 94: 12610-12615. The SR-BI knockout mouse provides proof of function for SR=BI in plasma HDL metabolism in vivo. In the absence of SR-BI, plasma HDL cholesterol accumulated in larger particles and adrenal glands are depleted of cholesterol.
33. Varban ML, Rinninger F, Wang N, Fairchild-Huntress V, Dunmore JH, Fang Q, et al. Targeted mutation reveals a central role of SR-BI in hepatic selective uptake of high density lipoprotein cholesterol. Proc Natl Acad Sci USA 1998; 95:4619-4624. An SR-BI mutation that reduces hepatic expression by 50% results in increased plasma HDL cholesterol. This is accompanied by a 50% reduction in the clearance of plasma HDL cholesteryl ester and a similar reduction in the selective uptake of HDL cholesteryl ester by the mouse liver.
34. Kozarsky KF, Donahee MH, Rigotti A, Iqbal SN, Edelman ER, Krieger M. Overexpression of the HDL receptor SR-BI alters plasma HDL and bile cholesterol levels. Nature 1997; 387:414-417.
35. Wang N, Arai T, Ji Y, Rinninger F, Tall AR. Liver- specific overexpression of scavenger receptor BI decreases levels of very low density lipoprotein apoB, low density lipoprotein apoB, and high density lipoprotein in transgenic mice. J Biol Chem 1998; 273:32920-32926. Hepatic overexpression of SR-BI produced the expected results in HDL metabolism: increased clearance of HDL cholesteryl ester and increased hepatic HDL cholesteryl ester selective uptake. Unexpectedly, SR-BI expression also reduced plasma LDL cholesteryl ester and largely prevented increases in apoB levels in response to high fat diets. These data indicate that, directly or indirectly, hepatic SR-BI influences the metabolism of apoB-containing lipoproteins.
36. Ueda Y, Royer L, Gong E, Zhang J, Cooper PN, Francone O, Rubin EM. Lower plasma levels and accelerated clearance of high density lipoprotein (HDL) and non-HDL cholesterol in scavenger receptor class B type I transgenic mice. J Biol Chem 1999; 274;7155-7171. Hepatic over expression of SR-BI reduced plasma HDL and non-HDL cholesterol and the level of plasma apoB. These effects were accompanied by an accelerated clearance of human LDL-apoB in reinjection experiments and a reduction in the sizes of endogenous apoB-containing lipoproteins. These data suggest that SR-BI may mediate selective cholesteryl ester uptake from LDL particles in vivo.
37. Rodrigueza WV, Thuahhia ST, Temel RE, Lund-Katz S, Rothblat G, Phillips MC, Williams DL. Mechanism of scanvenger receptor class B Type 1 (SR. B1)-mediated selective uptake of cholesteryl esters from high density lipoprotein to adrenal cells. J Biol Chem 1999; 274: 20344-20350. The SR-BI-mediated selective uptake of HDL cholesteryl ester occurs in proportion to the cholesteryl ester content of recombinant HDL particles and show a marked preference for cholesteryl ester as compared to most phospholipids, the exception being phosphatidylserine which is taken up equally to cholesteryl ester. The activation energy for selective upake of cholesteryl ester is low. These data lead to a model in which SR-BI forms a hydrophobic channel to permit HDL to the plasma membrane.
38. Calvo D, Gomez-Coronado D, Lasuncion MA, Vega MA. CLA-1 is an 85-kD plasma membrane glycoprotein that acts as a high-affinity receptor for both native (HDL, LDL, and VLDL) and modified (OxLDL and AcLDL) lipoproteins. Arterioscler Thromb Vasc Biol 1997; 17:2341-2349.
39. Pittman RC, Glass CK, Atkinson D, Small DM. Synthetic high density lipoprotein particles. Application to studies of the apoprotein specificity for selective uptake of cholesterol esters. J Biol Chem 1987; 262:2435-2442.
40. Xu S, Laccotripe M, Huang X, Rigotti A, Zannis VI, Krieger M. Apolipoproteins of HDL can directly mediate binding to the scavenger receptor SR-BI, an HDL receptor that mediates selective lipid uptake. J Lipid Res 1997; 38:1289-1298.
41. Williams DL, de la Llera-Moya M, Lund-Katz S, Connelly A, Thuahnai ST, Azhar GH, et al. Direct interaction between SR-BI and apoAI as determined by chemical cross-linking. Circulation 1998; 98:522.
42. Anantharamaiah GM, Jones JL, Brouillette CG, Schmidt CF, Chung BH, Hughes TA, et al. Studies of synthetic peptide analogs of the amphipathic helix. Structure of complexes with dimyristoyl phosphatidylcholine. J Biol Chem 1985; 260:10248-10255.
43. Connelly MA, Klein SM, Azhar S, Abumrad NA, Williams DL. Comparison of Class B scavenger receptors, CD36 and SR-BI, shows that both receptors mediate HDL-cholesteryl ester selective uptake but SR-BI exhibits a unique enhancement of cholesteryl ester uptake. J Biol Chem 1999; 274:41-47. This report leads to the hypothesis that HDL cholesteryl ester selective uptake results from two distinct steps. First, tethering the HDL particle to the cell surface by a class B scavenger receptor leads to a modest uptake of cholesteryl ester. Second, a marked facilitation of cholesteryl ester uptake occurs that is unique to SR-BI and requires the extracellular domain of the receptor. The data suggest that CD36 and SR-BII can mediate only the first step.
44. Gu X, Trigatti B, Xu S, Acton S, Babitt J, Krieger M. The efficient cellular uptake of high density lipoprotein lipide via scavenger receptor class B type I requires not only receptor-mediated suface binding but also receptor-specific lipid transfer mediated by its extracellular domain. J Biol Chem 1998; 273:26338-26348. This study shows that the extracellular domain of SR-BI is necessary for efficient uptake of HDL lipids in transfected cells. In addition, mutation of the major sites of fatty acylation had no effect on receptor clustering, HDL binding, or lipid uptake.
45. Brown MS, Goldstein JL. A receptor-mediated pathway far cholesterol homeostasis. Science 1986; 232:34-47.
46. Goldstein JL, Brown MS, Anderson RG, Russell DW, Schneider WJ. Receptor. mediated endocytosis: concepts emerging from the LDL receptor system. Annu Rev Cell Biol 1985; 1:1-39.
47. Krieger M, Herz J. Structures and functions of multiligand lipoprotein receptors; macrophage scavenger receptors and LDL receptor-related protein (LRP). Annu Rev Biochem 1994; 63:601-637.
48. Stangl H, Cao G, Wyne KL, Hobbs HH. Scavenger receptor, class B, type I-dependent stimulation of cholesterol esterification by high density lipoproteins, low density lipoproteins, and nonlipoprotein cholesterol. J Biol Chem 1998; 273:31002-31008. Evidence is presented that SR-BI-mediated cholesterol uptake occurs with LDL particles as judged by enhanced cholesterol esterification in transfected chinese hamster ovary cells. Interestingly, enhanced cholesterol esterification was seen with cholesterol aggregates or crystals suggesting that SR-BI can mediate free cholesterol uptake independently of interaction with lipoprotein particles.
49. Ji Y, Jian B, Wang N, Sun Y, de la Llera Moya M, Phillips GH, et al. Scavenger receptor Bi promotes high density lipoprotein-mediated cellular cholesterol efflux. J Biol Chem 1997; 272:20982-20985.
50. Jian B, de la Llera-Moya M, Ji Y, Wang N, Phillips MC, Swaney JB, et al. Scavenger receptor class B type I as a mediator of cellular cholesterol efflux to lipoproteins and phospholipid accepters. J Biol Chem 1998; 273:5599-5606. SR-BI was shown to mediate cellular free cholesterol efflux to phospholipid vesicle acceptors. In addition, among a variety of cell lines, the stimulation of free cholesterol efflux by phospholipid supplementation of human serum correlated with SR-BI expression levels.
51. de la Llers-Moya M, Rothblat GH, Coonelly MA, Kellner-Weiber G, Sakar SW, Phillips MC, Williams DL, Scavenger receptor BI (SR-BI) mediates free cholesterol flux independently of HDL tethering to the cell surface. J Lipid Res 1999; 40:575-580. These data lead to the hypothesis that a major component of SR-BI-stimulated free cholesterol efflux does not require binding of accepter particles to SR-BI. Rather, SR-BI expression alters plasma membrane lipid domains to faciltiate bidirectional free cholesterol flux.
52. Rothblat GH, de la Llera-Moya M, Atger V, Kellner-Weiber G, Williams DL, Phillips MC. Cell cholesterol efflux: integration of old and new observations provides new insights. JLipid Res 1999; 40:761-796.
53. Fukasawa M, Hirota K, Adachi H, Mimura K, Murakami-Murofushi K, Tsujimoto M, et al. Chinese hamser ovary cells expressing a novel type of acetylated low density lipoprotein receptor. J Biol Chem 1995; 270:1921-1927.
54. Fukasawa M, Adachi H, Hirers K, Tsujimoto M, Arai H, Inoue K. SRB1, a class B scavenger receptor, recognizes both negatively charged liposomes and apoptotic cells. Exp Cell Res 1996; 222:246-250.
55. Yancy PG, Rodrigueza WV, Kilsdonk EPC, Stoudt GW. Johnson WJ, Phillips MC, Rothblat GH. Cellular cholesterol efflux mediated by cyclodextrins: demonstration of kinetic pools and mechanism of efflux. J Biol Chem 1996; 271:16026-16034.
56. Brown D, London E. Structure and origin of ordered lipid domains in biological membranes. J Membr Biol 1996; 164:103-114.
57. Jacobsen K, Sheets ED, Simson R, Revisiting the fluid mosaic model of membranes. Science 1995; 268:1441-1442.
58. Schroeder F, Frolov AA, Murphy EJ, Atshaves BP, Jefferson JR, Pu L, et at. Recent advances in membrane cholesterol domain dynamics and intracellular cholesterol trafficking. Proc Soc Exp Biol Med 1996; 213:150-177.
59. Ahmed SN, Brown DA, London E. On the origin of sphingolipid/cholesterolrich detergent-insoluble Cell membranes; physiological concentrations of cholesterol and sphingolipid induce formation of a detergent-insoluble, liquid-ordered lipid phase in model membranes. Biochemistry 1997; 36:10944-10953.
60. Harder T, Simons K. Caveolae, DIGs, and the dynamics of sphingolipid-cholesterol microdomains. Curr Opin Cell Biol 1997; 9:534-542.
61. Lisanti MP, Scherer PE, Vidugiriene J, Tang Z, Hermanowski-Vosatka A, Tu Y-H, et al. Characterization of the caveolin-rich membrane domains isolated from an endothelial-rich source: implications for human disease. J Cell Biol 1994; 126:111-126.
62. Simionescu N, Lupu F, Simionescu M. Rings of membrane sterols surround the openings of vesicles and fenestrae, in capillary endothelium, J Cell Biol 1963; 97:1592-1600.
63. Chang W-J, Rothberg KG, Kamen BA, Anderson RGW. Lowering the cholesterol content of MA104 cells inhibits receptor-mediated transport of tolate, J Cell Biol 1992; 118:63-69.
64. Hailstones D, Sleer LS, Parton RG, Stanley KK. Regulation of caveolin and caveolae by cholesterol in MDCK cells. J Lipid Res 1998; 39:369-379.
65. Ilangumaran S, Hoessli DC. Effects of cholesterol depletion by cyclodextrin on the sphingolipid microdomains of the plasma membrane. Biochem J 1998; 335:433-440.
66. Fielding PE, Fielding CJ. Plasma membrane caveolae mediate the efflux et cellular free cholesterol. Biochemistry 1095; 34:14288-14292.
67. Graf GA, Connell PM, van der Westhuyzen DR, Smart EJ. The class B, type 1 scavenger receptor promotes the selective uptake of high density lipoprotein cholesteryl ethers into caveolae. J Biol Chem 1999; 274. HDL cholesteryl ethers are shown to transfer first into the ceveolar fraction in SR. BI-expressing Chinese hamster ovary cells before distribution to other membrane components. In addition, as much as 60% of the SR-BI was recovered in the caveolar fraction. These results suggest that the SR-BI-mediated selective uptake of HDL cholesteryl ester occurs via a caveolar route.
68. Smart EJ, Ying YS, Conrad PA, Anderson RGW. Caveolin moves from caveolae to the Golgi apparatus in response to cholesterol oxidation. J Cell Biol 1994; 127:1185-1197.
69. Knecht TP, Pittman RC. A plasma membrane pool of cholesteryl esters that may mediate the selective uptake of cholesteryl esters from high-density lipoproteins. Biochim Biophys Acta 1989; 1002:365-375.
70. Rinninger F, Jaeckle S, Pittman RC. A pool of reversibly cell-associated cholesteryl esters involved in the selctive uptake of cholesteryl esters tram high density lipoproteins by HepG2 hepatoma cells, Biochim Biophys Acta 1993; 1166:275-283.
71. Reaven E, Nomoto A, Leers-Sucheta S, Temel R, Williams DL, Azhar S. Expression and microvillar localization of scavenger receptor, class B, type I (a high density lipoprotein receptor) in luteinized and hormone-desensitized rat ovarian models, Endocrinology 1998; 139:2847-2856. Immunolocalization studies at the electron microscopic level show that SR-BI is localized to the cell surface microvilli and microvillar channels on rat luteal cells. These results provide further evidence that microvillar channels are a membrane compartment specialized for the selective uptake of lipoprotein cholesterol into steroidogenic cells.
72. Plump AS, Erickson SK, Wang W, Partin JS, Breslow JL Williams DL. Apolipoprotein A-I is required for cholesteryl ester accumulation in steroidogenic cells and for normal adrenal steroid production. J Clin Invest 1996; 97:2660-2671.
73. Williams DL, Wang JS, Wissig SL, Hamilton RL. Cell surface 'blanket' of apolipoprotein E on rat adrenocortical cells. J Lipid Res 1996; 36:745-758.
74. Azhar S, Nomoto A, Leers-Sucheta S, Reaven E. Simultaneous induction of an HDL receptor protein (SR-BI) and the selective uptake of HDL-cholesteryl esters in a physiologically relevant steroidogenic cell model. J Lipid Res 1998; 39:1616-1628. This work shows a tight and simultaneous hormonal induction of HDL cholesteryl ester selective uptake, SR-BI expression, and progestin synthesis in rat ovarian granulosa cells. Caveolin expression is decreased under the same conditions. Cholesterol loading of the cells with HDL has little or no effect on the SR-BI expresion level.
75. Reaven E, Lua Y, Nomoto A, Ternel R, Williams DL, van der Westhuyzen DR, Azhar S. The selective pathway and a high density lipoprotein receptor (SR-BI) in ovarian granulosa cells of the mouse. Biochim Biophys Acta 1999; 1436:565-576. SR-BI expression was dramatically induced by hormone treatment of mouse ovarian granulosa cells, but HDL cholesteryl ester selective uptake was only modestly increased. SR-BII expression was also induced by hormone, and caveolin expression was unchanged.
76. Hirano K, Nakagawa Y, Ohya T, Takamoto A, Matsuyama A, Okamoto Y, Matsumoto K, et al. Expression of CLA-1 in cultured human monocyte-derived macrophages and in human atherosclerotic lesions, Circulation 1998; 98:108.
77. Malveev SV, van der Westhuyzen DR, Smart EJ. The identification and biochemical characterization of macrophage caveolae. Circulation 1998; 98:384.
78. Trigatti B, Rayburn H, Vin̄als M, Braun A, Miettinen H, Penman M, et al. influence of the HDL receptor SE-BI on reproductive and cardiovascular pathophysiology. Proc Natl Acad Sci USA 1999; 96:9322-9327. This study demonstrates more rapid lesion development in the aortic root region of the apoE deficient moust in the absence of SR-BI providing evidence that SR-BI is athero-protective.
79. Arai T, Wang N, Bezouevski M,Welch C, Tall AR. Decreased atherosclerosis in heterezygous low density lipoprotein receptor-deficient mice expressing the scavenger receptor BI transgene. J Biol Chem 1999, 274:2366-2371. This study shows that hepatic overexpression of SR-BI in heterozygous LDL receptor knockout mice fed a high cholesterol/high fat/bile salt-containing diet reduced aortic root lesions. Depending on the diet, SR-BI expression reduced levels of both HDL and LDL cholesterol. The authors speculate that the athero- protective effects of SR-BI may reflect changes in the metabolism of apoB- containing lipoproteins.
80. Fluiter K, Sorrier W, De Beer MC, Connell PM, van der Westhuyzen DR, Van Berkel TJ. Scavenger receptor BI mediates the selective uptake of oxidized cholesterol esters by rat liver. J Biol Chem 1999; 274:8893-8899. This study shows that SR-BI mediates the efficient cellular uptake of oxidized cholesteryl esters from HDL. The authors propose that SR-BI is part of a transport system to remove lipid hydroperoxides thereby protecting LDL from oxidation.
81. Li X, Peegel H, Menon KMJ. In situ hybridization of high density lipoprotein (scavenger, type 1) receptor messenger ribonucleic acid (mRNA) during folliculogenesis and luteinization: evidence for mRNA expression and induction by human chorionic gonadotropin specifically in cell types that use cholesterol for steroidogenesis. Endocrinology 1998; 139:3043-3049. This report illustrates the hormonal induction of SR-BI mRNA in theca, interstitial, and luteal cells during follicular development and luteinization in rat ovary.
82. Parker KL, Schimmer BP. Steroidogenic factor 1: a key determinant of endocrine development and function. Endocr Rev 1997; 18:361-377.
83. Wang N, Weng W, Breslow JL, Tall AR. Scavenger receptor BI (SR-BI) is up-regulated in adrenal gland in apolipoprotein A-I and hepatic lipase knockout mice as a response to depletion of cholesterol stores. In vive evidence that SE-BI is a functional high density lipoprotein receptor under feedback control. J Biol Chem 1996; 271;21001-21004.
84. Spady DK, Woollett LA, Meidell RS, Hobbs HH. Kinetic characteristics and regulation of HDL cholesteryl ester and apolipoprotein transport in the apoA-I-/-mouse. J Lipid Res 1998; 39:1483-1492. SR-BI levels were shown to be the same in adrenal glands of wild type mice, apoA-I knockout mice, and apoA-I knockout mice in which plasma cholesterol levels were normalized by adenovirus-mediated expression of apoA-I. These data argue that, in comparison to the LDL receptor, adrenal SR-BI levels are relatively insensitive to changes in tissue and plasma cholesterol.
85. Fluiter K, van der Westhuijzen DR, Van Berkel TJ. In vive regulation of scavenger receptor BI and the selective uptake of high density lipoprotein cholesteryl esters in rat liver parenchymal and Kupffer cells. J Biol Chem 1998; 273:8434-8438. SR-BI expression was shown to be down-regulated in rat hepatocytes by either cholesterol feeding or ethinyl estradiol treatment. Kupffer cell SR-BI levels increased with both treatments.
86. Hatzopoulos AK, Rigotti A, Rosenberg RD, Krieger M. Temporal and spatial pattern of expression of the HDL receptor SR-BI during murine embryogenesis. J Lipid Res 1998; 39:495-508. This report describes the developmental pattern of SR-BI expression in tissues of the maternal/fetal interface. The authors speculate that SR-BI may facilitate lipid transfer to the developing embryo.
87. Wyne KL, Woollett LA. Transport of maternal LDL and HDL to the fetal membranes and placenta of the Golden Syrian hamster is mediated by receptor-dependent and receptor-independent processes. J Lipid Res 1998; 39:518-530. SR-BI and gp330 are shown to be expressed at high levels in the yolk sac of midgestation hamster embryos. Yolk sac shows a high level of HDL cholesteryl ester uptake and a similar uptake of HDL apoA-I, making it unclear whether cholesteryl ester is transported to the embryo by the selective uptake pathway.
88. Hauser H, Dyer JH, Nandy A, Vega MA, Warder M, Bieliauskaite E, et al. Identification of a receptor mediating absorption of dietary cholesterol in the intestine. Biochemistry 1998; 37: 17843-17850. Evidence is presented that SR-BI may be involved in the intestinal absorption of free cholesterol.
89. Shiratsuchi A, Kawasaki Y, Kemoto M, Rat H, Nakanishi Y. Rote of class B scavenger receptor type t in phagocytosis of apoptotic rat spermatogenic cells by Sertoli cells. J Biol Chem 1999; 274;5901-5908. SR-BI is shown to be expressed in Sertoli cells of the rat testis. The finding that antibody to SR-BI partially blocks the phagocytosis of apoptotic spermatogenic cells by Sertoli cells suggests that SR-BI may be responsible for the recognition of the apoptotic spermatogenic cells.
90. Illingworth DR, Lees AM, Lees RS. Adrenal cortical function in homozygous familial hypercholesterolemia. Metabol: Clin Exp 1983; 32:1045-1052.
91. Allen JM, Thompson GR, Myant NB. Normal adrenocortical response to adrenocorticotrophic hormone in patients with homozygous familial hypercholesterolemia. Clin Sci 1983; 65:99-101.
92. Boizel R, de Peretti E, Cathiard AM, Halimi S, Bost M, Berthezene F, Saez JM Pattern of plasma levels of cortisol, dehydoepiandrosterone and pregnenolone sulphate in normal subjects and in patients with homozygous familial hypercholesterolemia during ACTH infusion. Clin Endocrinol 1986; 25:363-371.
93. Laue L, Hoeg JM, Barnes K, Loriaux DL, Chrousos GP. The effect of mevinolin on steroidogenesis in patients with defects in the low density lipoprotein receptor pathway. J Clin Endocrinol Metab 1987; 64:531-535.
94. Illingworth DR, Kenny TA, Orwoll ES. Adrenal function in heterozygous and homozygous hypobetalipoproteinemia. J Clin Endocrinol Metab 1982; 54:27-33.
95. Illingworth DR, Orwoll ES, Conner WE. Impaired cortisol secretion in abetalipoproteinemia. J Clin Endocrinol Metab 1980; 50:977-979.
96. Sorci Thomas M, Rudel LL. Intravascular metabolism of lipoprotein cholesteryl esters in African green monkeys: differential fate of doubly labeled cholesteryl oleate. J Lipid Res 1997; 28:572-581.
97. Scobey MW, Johnson FL, Rudel LL. Delivery of high-density lipoprotein free and esterified cholesterol to bile by the perfused monkey liver. Am J Physiol 1989; 257:G644-G652.