Characterization of CLA-1, a Human Homologue of Rodent Scavenger Receptor BI, as a Receptor for High Density Lipoprotein and Apoptotic Thymocytes

Murao, Koji; Terpstra, Valeska; Green, Simone R.; Kondratenko, Nonna; Steinberg, Daniel; Quehenberger, Oswald

doi:10.1074/jbc.272.28.17551

Cited by 309 publications

(305 citation statements)

References 44 publications

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“…[24][25][26][27] At least two distinct ligand-binding sites have been reported to exist on the SR-BI molecule. 23,28 To further understand the role of SR-BI in HCV-cell entry, we investigated the effects of SR-BI ligands on viral infectivity.…”

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confidence: 99%

Oxidized low-density lipoprotein inhibits hepatitis C virus cell entry in human hepatoma cells

et al. 2006

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confidence: 99%

Oxidized low-density lipoprotein inhibits hepatitis C virus cell entry in human hepatoma cells

et al. 2006

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“…The scavenger receptor class B type I (SR-BI) is a cell surface receptor expressed predominantly in liver and steroidogenic tissues (i.e., testis, ovaries, and adrenals) (5)(6)(7)(8) that mediates the selective uptake of cholesteryl esters from HDL without the concomitant uptake and degradation of the HDL particle (6). Studies by Temel et al (9) have shown that SR-BI serves as the major route for the selective uptake of HDL cholesteryl esters and for the delivery of HDL cholesterol to the steroidogenic pathway in cultured adrenal cells in vitro.…”

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confidence: 99%

Absence of HDL cholesteryl ester uptake in mice via SR-BI impairs an adequate adrenal glucocorticoid-mediated stress response to fasting

Hoekstra¹,

Meurs²,

Koenders³

et al. 2008

Journal of Lipid Research

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Receptor-mediated cholesterol uptake has been suggested to play a role in maintaining the adrenal intracellular free cholesterol pool and the ability to produce hormones. Therefore, in the current study, we evaluated the importance of scavenger receptor class B type I (SR-BI)-mediated cholesteryl ester uptake from HDL for adrenal glucocorticoid hormone synthesis in vivo. No difference was observed in the plasma level of corticosterone between SR-BI-deficient and wild-type mice under ad libitum feeding conditions. Overnight fasting (?16 h) stimulated the plasma level of corticosterone by 2-fold in wild-type mice. In contrast, no effect of fasting on plasma corticosterone levels was observed in SR-BI-deficient mice, leading to a 44% lower plasma corticosterone level compared with their wild-type littermate controls. In parallel, an almost complete depletion of lipid stores in the adrenal cortex of fasted SR-BIdeficient mice was observed. Plasma adrenocorticotropic hormone levels were increased by 5-fold in fasted SR-BIdeficient mice. SR-BI deficiency induced marked changes in the hepatic expression of the glucocorticoid-responsive genes cholesterol 7a-hydroxylase, HMG-CoA synthase, apolipoprotein A-IV, corticosteroid binding globulin, interleukin-6, and tumor necrosis factor-a, which coincided with a 42% decreased plasma glucose level under fasting conditions. In conclusion, we show that the absence of adrenal HDL cholesteryl ester uptake in SR-BI-deficient mice impairs the adrenal glucocorticoid-mediated stress response to fasting as a result of adrenal glucocorticoid insufficiency and attenuated liver glucocorticoid receptor signaling, leading to hypoglycemia under fasting conditions.-Hoekstra, M., I. Meurs, M. Koenders, R. Out, R. B. Hildebrand, J. K. Kruijt, M. Van Eck, and T. J. C. Van Berkel. Absence of HDL cholesteryl ester uptake in mice via SR-BI impairs an adequate adrenal glucocorticoid-mediated stress response to fasting. J. Lipid Res. 2008. 49: 738-745.

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“…Cells were washed, scraped in PBS and lysed as described previously [15]. The membranes were incubated for 1 h at 4°C with 0.2% Tween 20 in PBS containing anti-PREB antiserum (diluted 1:250) as described previously [3].…”

Section: Western Blot Analysismentioning

confidence: 99%

Prolactin regulatory element binding protein as a potential transcriptional factor for the insulin gene in response to glucose stimulation

et al. 2006

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Aims/hypothesis: Prolactin regulatory element binding (PREB) protein has been identified as a factor that regulates prolactin promoter activity in rat anterior pituitary. PREB is located not only in the anterior pituitary but also in pancreas; however its role in the pancreas is not known. We therefore examined the role of PREB in insulin gene expression. Materials and methods: To analyse the effects of PREB on insulin gene transcription, we employed the luciferase reporter gene assay and electrophoretic mobility shift assay (EMSA). In cells expressing or knocked down for PREB, insulin expression and secretion were determined. Results: PREB was located mainly in nuclei of rat pancreatic beta cells and its cell line, INS-1. A nuclear extract of INS-1 cells contained material that was recognised by PREB antiserum. This nuclear extract also showed insulin promoter binding activity that was super-shifted by PREB antiserum in EMSA studies. In the INS-1 cells, co-expression of PREB and the insulin promoter induced activity of the latter. The addition of glucose to the cells increased PREB expression. Deletional analysis of the insulin promoter showed that A3, a glucose-responsive cis-element in the insulin promoter, mediated the transcriptional effect of PREB. In addition, synthesised PREB bound the A3 element by EMSA, while a mutant of this motif in the insulin promoter abrogated the effect of PREB. Cells expressing or knocked down for PREB exhibited increased or decreased insulin expression, respectively. Conclusions/interpretation: These results demonstrate that PREB may contribute to the regulation of insulin gene transcription and insulin secretion in response to glucose stimulation.

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Characterization of CLA-1, a Human Homologue of Rodent Scavenger Receptor BI, as a Receptor for High Density Lipoprotein and Apoptotic Thymocytes

Cited by 309 publications

References 44 publications

Oxidized low-density lipoprotein inhibits hepatitis C virus cell entry in human hepatoma cells

Oxidized low-density lipoprotein inhibits hepatitis C virus cell entry in human hepatoma cells

Absence of HDL cholesteryl ester uptake in mice via SR-BI impairs an adequate adrenal glucocorticoid-mediated stress response to fasting

Prolactin regulatory element binding protein as a potential transcriptional factor for the insulin gene in response to glucose stimulation

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