Редактирование: ABCG5 (раздел)

==Publications==

{{medline-entry
|title=2, 3, 4', 5-tetrahydroxystilbene-2-0-β-d Glycoside Attenuates Age- and Diet-Associated Non-Alcoholic Steatohepatitis and Atherosclerosis in LDL Receptor Knockout Mice and Its Possible Mechanisms.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30939745
|abstract=The compound, 2,3,5,4'-tetrahydroxystilbene-2-O-β-d-glucoside (TSG), a primary bioactive polyphenolic component of [i]Polygonum multiflorum[/i] exerts numerous pharmacological activities. However, its protective effect against non-alcoholic steatohepatitis (NASH), in the context of metabolic syndrome, remains poorly understood. The aim of the present study is to evaluate the effects of TSG treatment on middle-aged (12-mo-old) male LDLr  mice, which were fed a high fat diet for 12 weeks to induce metabolic syndrome and NASH. At the end of the experiment, the blood samples of mice were collected for determination of metabolic parameters. Liver and aorta tissues were collected for analysis, such as histology, immunofluorescence, hepatic lipid content, real-time PCR, and western blot. Our data show that TSG treatment improved the different aspects of NASH (steatosis, inflammation, and fibrosis) and atherosclerosis, as well as some of the metabolic basal characteristics. These modulatory effects of TSG are mediated, at least in part, through regulating key regulators of lipid metabolism (SREBP1c, PPARα and their target genes, [[ABCG5]] and CYP7A1), inflammation (CD68, [[TNF]]-α, IL-6 and ICAM), fibrosis (α-SMA and [[TNF]]β) and oxidative stress (NADPH-oxidase 2/4, [[CYP2E1]] and antioxidant enzymes). These results suggest that TSG may be a promising candidate for preventing and treating the progression of NASH.
|mesh-terms=* Aging
* Animals
* Aorta
* Atherosclerosis
* Diet, High-Fat
* Glucosides
* Lipid Metabolism
* Liver
* Male
* Mice
* Mice, Inbred C57BL
* Non-alcoholic Fatty Liver Disease
* Receptors, LDL
* Stilbenes
|keywords=* atherosclerosis
* metabolic syndrome
* nonalcoholic steatohepatitis
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6479705
}}
{{medline-entry
|title=Genetic determinants of macular pigments in women of the Carotenoids in Age-Related Eye Disease Study.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23404124
|abstract=To investigate genetic determinants of macular pigment optical density in women from the Carotenoids in Age-Related Eye Disease Study (CAREDS), an ancillary study of the Women's Health Initiative Observational Study. 1585 of 2005 CAREDS participants had macular pigment optical density (MPOD) measured noninvasively using customized heterochromatic flicker photometry and blood samples genotyped for 440 single nucleotide polymorphisms (SNPs) in 26 candidate genes related to absorption, transport, binding, and cleavage of carotenoids directly, or via lipid transport. SNPs were individually tested for associations with MPOD using least-squares linear regression. Twenty-one SNPs from 11 genes were associated with MPOD (P ≤ 0.05) after adjusting for dietary intake of lutein and zeaxanthin. This includes variants in or near genes related to zeaxanthin binding in the macula (GSTP1), carotenoid cleavage (BCMO1), cholesterol transport or uptake (SCARB1, [[ABCA1]], [[ABCG5]], and LIPC), long-chain omega-3 fatty acid status (ELOVL2, [[FADS1]], and FADS2), and various maculopathies (ALDH3A2 and RPE65). The strongest association was for rs11645428 near BCMO1 (βA = 0.029, P = 2.2 × 10(-4)). Conditional modeling within genes and further adjustment for other predictors of MPOD, including waist circumference, diabetes, and dietary intake of fiber, resulted in 13 SNPs from 10 genes maintaining independent association with MPOD. Variation in these single gene polymorphisms accounted for 5% of the variability in MPOD (P = 3.5 × 10(-11)). Our results support that MPOD is a multi-factorial phenotype associated with variation in genes related to carotenoid transport, uptake, and metabolism, independent of known dietary and health influences on MPOD.
|mesh-terms=* Aged
* Aged, 80 and over
* Aging
* Carotenoids
* Cross-Sectional Studies
* Female
* Humans
* Macular Degeneration
* Phenotype
* Polymorphism, Single Nucleotide
* Postmenopause
* Retinal Pigments
* Scavenger Receptors, Class B
* beta-Carotene 15,15'-Monooxygenase

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3626525
}}
{{medline-entry
|title=Distinct spatio-temporal expression of ABCA and ABCG transporters in the developing and adult mouse brain.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/16181433
|abstract=Using in situ hybridization for the mouse brain, we analyzed developmental changes in gene expression for the ATP-binding cassette (ABC) transporter subfamilies [[ABCA1]]-4 and 7, and [[ABCG1]], 2, 4, 5 and 8. In the embryonic brains, [[ABCA1]] and A7 were highly expressed in the ventricular (or germinal) zone, whereas [[ABCA2]], A3 and G4 were enriched in the mantle (or differentiating) zone. At the postnatal stages, [[ABCA1]] was detected in both the gray and white matter and in the choroid plexus. On the other hand, [[ABCA2]], A3 and A7 were distributed in the gray matter. In addition, marked up-regulation of [[ABCA2]] occurred in the white matter at 14 days-of-age when various myelin protein genes are known to be up-regulated. In marked contrast, [[ABCA4]] was selective to the choroid plexus throughout development. [[ABCG1]] was expressed in both the gray and white matters, whereas [[ABCG4]] was confined to the gray matter. [[ABCG2]] was diffusely and weakly detected throughout the brain at all stages examined. Immunohistochemistry of [[ABCG2]] showed its preferential expression on the luminal membrane of brain capillaries. Expression signals for [[ABCG5]] and G8 were barely detected at any stages. The distinct spatio-temporal expressions of individual ABCA and G transporters may reflect their distinct cellular expressions in the developing and adult brains, presumably, to regulate and maintain lipid homeostasis in the brain.
|mesh-terms=* ATP-Binding Cassette Transporters
* Aging
* Animals
* Animals, Newborn
* Brain
* Embryo, Mammalian
* Immunohistochemistry
* In Situ Hybridization
* Mice
* Mice, Inbred C57BL
* Tissue Distribution

|full-text-url=https://sci-hub.do/10.1111/j.1471-4159.2005.03369.x
}}