The human ABCG1 gene: identification of LXR response elements that modulate expression in macrophages and liver

Sabol, Steven L.; Brewer, H. Bryan; Santamarina-Fojo, Silvia

doi:10.1194/jlr.m500080-jlr200

Cited by 135 publications

(86 citation statements)

References 62 publications

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“…We measured ABCG1 protein levels in the PM fraction to find that, under the knockdown of ABCG1, ABCG1 expression was markedly attenuated by glibenclamide in PM as compared to WC. Our ABCG1 overexpression study confirmed the previous observation that such manipulation induced a slight but significant increase in HDL-mediated cholesterol efflux 4) . Additionally, in the presence of Ad-hABCG1, high-dose glibenclamide promoted HDL-mediated cholesterol efflux to a similar extent to that in the control virus (13% in control virus vs. 12% in Ad-ABCG1); however, it was puzzling that glibenclamide substantially decreased the originally overexpressed ABCG1 protein levels in WC.…”

Section: High-dose Glibenclamide Promotes Hdl-mediated Efflux Indepensupporting

confidence: 81%

“…Liver X receptor-responsive elements (LXRE), direct repeat spaced by four nucleotides, were present in hABCA1 940 110 and hABCG1A 1104 37, but not in hABCG1B 1180 144, as previously reported 2,4) .…”

Section: Construction Of Luciferase Reporter Plasmidssupporting

confidence: 58%

“…Luciferase reporter plasmids (pGL3 Basic; Promega, Madison, WI) containing the human ABCA1 promoter region spanning 940 to 110 bp (hABCA1 940 110), the human ABCG1 promoter A spanning 1104 to 37 bp (located upstream of exon 1, hABCG1A 1104 37), and promoter B spanning 1180 to 144 bp (located upstream of exon 5, hABCG1B 1180 144) were generated as previously reported [1][2][3][4] . Liver X receptor-responsive elements (LXRE), direct repeat spaced by four nucleotides, were present in hABCA1 940 110 and hABCG1A 1104 37, but not in hABCG1B 1180 144, as previously reported 2,4) .…”

Section: Construction Of Luciferase Reporter Plasmidsmentioning

confidence: 99%

“…ATP binding cassette transporter A1 (ABCA1) has been shown to play an important role in apolipoprotein A-I (apoA-I)-mediated cholesterol efflux from peripheral cells and macrophages 2,3) . Further, ATP binding cassette transporter G1 (ABCG1) and scavenger receptor class B type I (SR-BI) promote cholesterol efflux from mac-rophages to HDL particles but not to lipid-poor apoA- 4,5) , and thus work in concert to facilitate the cholesterol efflux reaction through a wide range of HDL subspecies.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Sulfonylurea Agents on Reverse Cholesterol Transport in Vitro and Vivo

Terao

Ayaori

Ogura

et al. 2011

JAT

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Section: High-dose Glibenclamide Promotes Hdl-mediated Efflux Indepensupporting

confidence: 81%

Section: Construction Of Luciferase Reporter Plasmidssupporting

confidence: 58%

Section: Construction Of Luciferase Reporter Plasmidsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Effect of Sulfonylurea Agents on Reverse Cholesterol Transport in Vitro and Vivo

Terao

Ayaori

Ogura

et al. 2011

JAT

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“…The luciferase reporter construct LXRE×3-TK-LUC was transiently transfected without or with pcDNA3, pcDNA3-hLXRα or pcDNA3-hLXRβ [22] into HIT-T15 or MIN6 cells grown in 24 well plates using the Lipofectamine 2000 reagent according to the manufacturer's instructions. A plasmid expressing the gene encoding β-galactosidase driven by the cytomegalovirus (CMV) promoter (Clontech Laboratories, Palo Alto, CA, USA) was simultaneously cotransfected as an internal control.…”

Section: Transient Transfection and Luciferase Reporter Assaymentioning

confidence: 99%

Activation of liver X receptors inhibits pancreatic islet beta cell proliferation through cell cycle arrest

et al. 2008

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Aims/hypothesis Liver X receptors (LXRs) are important transcriptional regulators of lipid homeostasis and proliferation in several cell types. However, the roles of LXRs in pancreatic beta cells have not been fully established. The aim of this study was to investigate the effects of LXRs on pancreatic beta cell proliferation. Methods Gene expression was analysed using real-time RT-PCR. Transient transfection and reporter gene assays were used to determine the transcriptional activity of LXRs in pancreatic beta cells. Cell viability and proliferation were analysed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), DNA fluorometric, BrdU labelling and [3 H]thymidine incorporation assays. Cell cycle distribution was investigated by flow cytometry analysis. Adenovirus-based RNA interference was used to knockdown LXRα, LXRβ and p27 in MIN6 cells and mouse islets.Results We found that both Lxrα (also known as Nr1h3) and Lxrβ (also known as Nr1h2) were expressed and transactivated the LXR response element in HIT-T15 and MIN6 cells. Activation of LXRs dose-dependently inhibited pancreatic beta cell viability and proliferation. This was accompanied by beta cell cycle arrest at the G1 phase. Furthermore, LXR activation increased levels of the p27 protein by inhibiting its degradation. Knockdown of p27 reversed these effects of LXR activation on growth inhibition and cell cycle arrest. Conclusions/interpretation Our observations indicate that LXR activation inhibits pancreatic beta cell proliferation through cell cycle arrest. A well-known regulator of pancreatic beta cell cycle progression, p27, is upregulated and mediates the effects of LXRs on growth inhibition in beta cells. These observations suggest the involvement of aberrant activation of LXR in beta cell mass inadequacy, which is an important step in the development of type 2 diabetes.Keywords Beta cell . Cell cycle . Islet . LXR . p27 . Proliferation Abbreviations CMV cytomegalovirus GFP green fluorescent protein LXR liver X receptor LXRE liver X receptor response element MTT 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide RNAi RNA interference SKP2 S-phase kinase-associated protein 2 siRNA small interfering RNA

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Regulation of Genes Involved in the Biogenesis and the Remodeling of HDL

Kardassis

Drosatos

Zannis

2007

High‐Density Lipoproteins

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The human ABCG1 gene: identification of LXR response elements that modulate expression in macrophages and liver

Cited by 135 publications

References 62 publications

Effect of Sulfonylurea Agents on Reverse Cholesterol Transport in Vitro and Vivo

Effect of Sulfonylurea Agents on Reverse Cholesterol Transport in Vitro and Vivo

Activation of liver X receptors inhibits pancreatic islet beta cell proliferation through cell cycle arrest

Regulation of Genes Involved in the Biogenesis and the Remodeling of HDL

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