Abstract
The genomics of atherosclerosis can arise as a result of cross-talk between the genes coding for the LDL-receptor (LDL-R), LXR-alpha, PPARs (alpha, gamma), CD36 and C-myc because these genes control lipid metabolism, cytokine production and cellular activity within the arterial wall. The effect of green tea polyphenols (GTPs) upon such genomics revealed their ability to down-regulate genes coding for PPAR-gamma, CD36, LXR-alpha, C-myc coupled with up-regulation of genes coding for LDL-R and PPAR-alpha at the transcriptional level. Based upon these results, it is proposed that GTPs have the inherent capacity to inhibit the development of atherosclerotic lesions.
Copyright 2004 John Wiley & Sons, Ltd.
MeSH terms
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Arteriosclerosis / genetics*
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Arteriosclerosis / prevention & control*
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DNA-Binding Proteins
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Dose-Response Relationship, Drug
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Flavonoids / administration & dosage
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Flavonoids / pharmacology*
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Flavonoids / therapeutic use
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Gene Expression Regulation
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Genes, myc / genetics
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Humans
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Leukocytes, Mononuclear / drug effects
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Liver X Receptors
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Orphan Nuclear Receptors
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Phenols / administration & dosage
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Phenols / pharmacology*
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Phenols / therapeutic use
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Phytotherapy*
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Polyphenols
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Receptors, Cytoplasmic and Nuclear / drug effects
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Receptors, Cytoplasmic and Nuclear / genetics
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Receptors, LDL / genetics
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Tea*
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Transcription Factors / genetics
Substances
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DNA-Binding Proteins
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Flavonoids
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Liver X Receptors
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NR1H3 protein, human
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Orphan Nuclear Receptors
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Phenols
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Polyphenols
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Receptors, Cytoplasmic and Nuclear
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Receptors, LDL
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Tea
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Transcription Factors