Expression of the ATP-Binding Cassette Transporter Gene ABCG1 (ABC8) in Tangier Disease

Lorkowski, Stefan; Kratz, Mario; Wenner, Claudia; Schmidt, Roland; Weitkamp, Benedikt; Fobker, Manfred; Reinhardt, Jürgen; Rauterberg, Jürgen; Galinski, Erwin A.; Cullen, Paul

doi:10.1006/bbrc.2001.4863

Cited by 62 publications

(51 citation statements)

References 39 publications

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“…The present results indicate that, in Japanese men, the presence of the G allele of 257T G polymorphism on the ABCG1 gene confers an appreciable increase in the risk of multi-vessel CAD. ABCG1 is upregulated in macrophages of patients with Tangier's disease, which is caused by a defect in the ABCA1 gene, suggesting cooperative ABCA1 and ABCG1 regulation and a role of the two subfamilies in lipid homeostasis 25) . Although the mechanism remains elusive, the ABCG1 transporter may potentially assume an important function in HDL lipidation 10,11) .…”

Section: Discussionmentioning

confidence: 99%

Genotypic Effect of ABCG1 Gene Promoter -257T>G Polymorphism on Coronary Artery Disease Severity in Japanese Men

Furuyama

Uehara

Zhang

et al. 2009

JAT

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Aim: ATP-binding cassette transporter G1 (ABCG1) is a cholesterol transporter that plays a role in cholesterol efflux in the presence of high-density lipoprotein (HDL). Moreover, HDL-mediated cholesterol efflux is increased in cultured ABCG1 overexpressed cells; however, the physiological roles of ABCG1 and its contribution to atherosclerosis in humans remain unclear. Methods: The effect of ABCG1 257T G mutation on transcription activity was determined by a reporter assay. One hundred nine Japanese men with coronary artery disease (CAD) were analyzed. ABCG1 257T G polymorphism was assessed by mutation-selective PCR methods to identify T/T, T/G, and G/G genotypes. Results:The reporter assay showed that ABCG1 transcription activity was significantly lower (p 0.01) in the G allele of 257T G polymorphism compared with that in the T allele. Clinically, there were no significant differences in serum triglyceride and total, LDL, and HDL cholesterol levels, or other risk factors. Logistic regression analysis revealed significant additive and dominant effects on the frequency of patients with multi-vessel disease compared with single-vessel disease

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Section: Discussionmentioning

confidence: 99%

Genotypic Effect of ABCG1 Gene Promoter -257T>G Polymorphism on Coronary Artery Disease Severity in Japanese Men

Furuyama

Uehara

Zhang

et al. 2009

JAT

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“…The intracellular contents of free cholesterol, total cholesterol, and phospholipids of HEK/ABCG1 were 15 6 0.73, 16 6 0.58, and 61 6 0.50 mg/well, respectively, and not significantly different from those of HEK293 host cells. Therefore, 5.5% and 1.5% of cellular total cholesterol and phospholipids were 1, 4, 7, 10, 13, 16), HEK/ABCG1 cells (lanes 2,5,8,11,14,17), and HEK/ABCG1-K120M cells (lanes 3,6,9,12,15,18) were treated without (lanes 1-6) or with dithiobis (succinimidylpropionate) (DSP; lanes 7-12) or dimethyl 3,39-dithiobispropionimidate-HCl (DTBP; lanes [13][14][15][16][17][18]. Cell lysates (20 mg of protein) were treated without (lanes 1-3, 7-9, 13-15) or with DTT (lanes 4-6, 10-12, 16-18).…”

Section: Efflux Of Cholesterol and Phospholipids By Abcg1mentioning

confidence: 99%

“…Human ABCG1 cDNA was cloned as a gene homologous to white in Drosophila (6), a transporter of eye pigments, and many N-terminal variant forms of ABCG1 have been reported (7,8). Other members of the ABCG subfamily form a dimer to function.…”

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confidence: 99%

Efflux of sphingomyelin, cholesterol, and phosphatidylcholine by ABCG1

Kobayashi

Takanezawa

Hirata

et al. 2006

Journal of Lipid Research

185

147

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Cholesterol and phospholipids are essential to the body, but an excess of cholesterol or lipids is toxic and a risk factor for arteriosclerosis. ABCG1, one of the halftype ABC proteins, is thought to be involved in cholesterol homeostasis. To explore the role of ABCG1 in cholesterol homeostasis, we examined its subcellular localization and function. ABCG1 and ABCG1-K120M, a WalkerA lysine mutant, were localized to the plasma membrane in HEK293 cells stably expressing ABCG1 and formed a homodimer. A stable transformant expressing ABCG1 exhibited efflux of cholesterol and choline phospholipids in the presence of BSA, and the cholesterol efflux was enhanced by the presence of HDL, whereas cells expressing ABCG1-K120M did not, suggesting that ATP binding and/or hydrolysis is required for the efflux. Mass and TLC analyses revealed that ABCG1 and ABCA1 secrete several species of sphingomyelin (SM) and phosphatidylcholine (PC), and SMs were preferentially secreted by ABCG1, whereas PCs were preferentially secreted by ABCA1. These results suggest that ABCA1 and ABCG1 mediate the lipid efflux in different mechanisms, in which different species of phospholipids are secreted, and function coordinately in the removal of cholesterol and phospholipids from peripheral

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“…4B). Figure 4C shows the genomic organization and reported transcripts (19,20) of human ABCG1. We recently investigated the relative contributions of promoters A and B (located upstream of exons 1 and 5, respectively) in macrophages and found that the activity of promoter B was substantially greater than that of promoter A (7).…”

Section: Astaxanthin Transcriptionally Induces Abca1 and Abcg1 Expresmentioning

confidence: 99%

Astaxanthin Enhances ATP-Binding Cassette Transporter A1/G1 Expressions and Cholesterol Efflux from Macrophages

Iizuka

Ayaori

Uto‐Kondo

et al. 2012

J Nutr Sci Vitaminol

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Summary ATP-binding cassette transporters (ABC) A1 and G1 are key molecules in cholesterol efflux from macrophages, which is an initial step of reverse cholesterol transport (RCT), a major anti-atherogenic property of high-density lipoprotein (HDL). Astaxanthin is one of the naturally occurring carotenoids responsible for the pink-red pigmentation in a variety of living organisms. Although astaxanthin is known to be a strong antioxidant, it remains unclear through what mechanism of action it affects cholesterol homeostasis in macrophages. We therefore investigated the effects of astaxanthin on cholesterol efflux and ABCA1/G1 expressions in macrophages. Astaxanthin enhanced both apolipoprotein (apo) A-I-and HDL-mediated cholesterol efflux from RAW264.7 cells. In supporting these enhanced cholesterol efflux mechanisms, astaxanthin promoted ABCA1/G1 expression in various macrophages. In contrast, peroxisome proliferator-activated receptor ␥ , liver X receptor (LXR) ␣ and LXR ␤ levels remained unchanged by astaxanthin. An experiment using actinomycin D demonstrated that astaxanthin transcriptionally induced ABCA1/G1 expression, and oxysterol depletion caused by overexpression of cholesterol sulfotransferase further revealed that these inductions in ABCA1/G1 were independent of LXR-mediated pathways. Finally, we performed luciferase assays using human ABCA1/G1 promoterreporter constructs to reveal that astaxanthin activated both promoters irrespective of the presence or absence of LXR-responsive elements, indicating LXR-independence of these activations. In conclusion, astaxanthin increased ABCA1/G1 expression, thereby enhancing apoA-I/HDL-mediated cholesterol efflux from the macrophages in an LXR-independent manner. In addition to the anti-oxidative properties, the potential cardioprotective properties of astaxanthin might therefore be associated with an enhanced anti-atherogenic function of HDL.

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Expression of the ATP-Binding Cassette Transporter Gene ABCG1 (ABC8) in Tangier Disease

Cited by 62 publications

References 39 publications

Genotypic Effect of ABCG1 Gene Promoter -257T>G Polymorphism on Coronary Artery Disease Severity in Japanese Men

Genotypic Effect of ABCG1 Gene Promoter -257T>G Polymorphism on Coronary Artery Disease Severity in Japanese Men

Efflux of sphingomyelin, cholesterol, and phosphatidylcholine by ABCG1

Astaxanthin Enhances ATP-Binding Cassette Transporter A1/G1 Expressions and Cholesterol Efflux from Macrophages

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