Tetrahydrocortisol–apolipoprotein A-I complex specifically interacts with eukaryotic DNA and GCC elements of genes

Панин, Л. Е.; Тузиков, Ф. В.; Gimautdinova, O. I.

doi:10.1016/j.jsbmb.2003.09.004

Cited by 11 publications

(26 citation statements)

References 18 publications

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“…Whether and how these responses relate to the observed differences in epigenetic effects between HDL-rich and -poor lipoprotein mixes and among individual lipoproteins cannot be concluded at present (1). Notably, we detected ApoA-I, a major HDL constituent, in nuclear preparations of HDL-stimulated cells in accordance with previous reports suggesting that HDL-derived factors may well operate as nuclear factors (2,16). This idea is supported by recent evidence that the HDL atypical apolipoprotein ApoD can be detected within the nuclear space (17,18).…”

Section: Discussionsupporting

confidence: 87%

Apolipoprotein B epitopes are present in nuclear preparations of human and mouse cells

Døssing

Zaina²

2009

Int J Mol Med

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Abstract. We previously showed that a native very lowdensity lipoprotein (VLDL)-and low-density lipoprotein (LDL)-rich mix induces global changes in DNA methylation in cultured THP-1 human macrophages. The exact molecular mechanisms for this response are not yet known. Previous studies showed that apolipoprotein B (ApoB) or its fragments can be localized in nuclei following cellular uptake, thus suggesting that ApoB may have a chromatin-modifying activity. To verify this hypothesis, we assessed whether ApoB epitopes are detected in THP-1 and mouse cell nuclei. Using a combination of immunoblotting, immunocytochemistry and chromatin immunoprecipitation, we showed that ApoB epitopes are present in THP-1 cell and mouse monocyte/ macrophage nuclear fractions, but are perinuclear rather than intranuclear. Our results are not consistent with a direct chromatin-ApoB interaction as an underlying mechanism for the observed epigenetic responses to lipoproteins in THP-1 cells.

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Section: Discussionsupporting

confidence: 87%

Apolipoprotein B epitopes are present in nuclear preparations of human and mouse cells

Døssing

Zaina²

2009

Int J Mol Med

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“…The mechanisms by which lipoproteins can affect DNA methylation patterns are currently not understood. APOA-I, a constituent of HDL, is physically associated with active chromatin and binds to a CG-rich oligonucleotide in vitro, suggesting a role for lipoprotein constituents in chromatin binding and remodeling (50,51). Further studies are necessary to elucidate the functional consequences of these interactions in atherogenesis.…”

Section: Discussionmentioning

confidence: 99%

DNA Methylation Polymorphisms Precede Any Histological Sign of Atherosclerosis in Mice Lacking Apolipoprotein E

Lund¹,

Andersson

Lauria³

et al. 2004

Journal of Biological Chemistry

295

202

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The present work investigates the occurrence and significance of aberrant DNA methylation patterns during early stages of atherosclerosis. To this end, we asked whether the genetically atherosclerosis-prone APOEnull mice show any changes in DNA methylation patterns before the appearance of histologically detectable vascular lesion. We exploited a combination of various techniques: DNA fingerprinting, in vitro methyl-accepting assay, 5-methylcytosine quantitation, histone posttranslational modification analysis, Southern blotting, and PCR. Our results show that alterations in DNA methylation profiles, including both hyper-and hypomethylation, were present in aortas and PBMC of 4-week-old mutant mice with no detectable atherosclerotic lesion. Sequencing and expression analysis of 60 leukocytic polymorphisms revealed that epigenetic changes involve transcribed genic sequences, as well as repeated interspersed elements. Furthermore, we showed for the first time that atherogenic lipoproteins promote global DNA hypermethylation in a human monocyte cell line. Taken together, our results unequivocally show that alterations in DNA methylation profiles are early markers of atherosclerosis in a mouse model and may play a causative role in atherogenesis.Atherosclerosis and its complications are a major cause of death and disability in the developed world. The disease is characterized by infiltration of lipid particles in the arterial wall, accompanied by the recruitment of inflammatory and immune cells, migration and proliferation of smooth muscle cells (SMC), 1 and synthesis of extracellular matrix. These processes eventually result in the gradual development of an elevated lipid-rich, fibrocellular lesion (1).In mammals, DNA methyltransferases use S-adenosyl methionine (SAM) as a methyl group donor to methylate the carbon in position 5 of cytosine residues in a CpG dinucleotide (CG) context (2). DNA methylation regulates fundamental biological phenomena such as gene expression, genome stability, mutation rate, genomic imprinting, and X chromosome inactivation (3-6). Both global and gene-specific alterations in DNA methylation are associated with abnormal phenotypes in disease (7,8). For example, cancer cells show global genomic hypomethylation and dense hypermethylation of CpG islands, which are normally unmethylated (9). The identification of cancer type-and stage-specific changes in DNA methylation has justified hopes for novel diagnostic and therapeutic avenues (10).Two general observations suggest that alterations in DNA methylation patterns are involved in atherogenesis (11-13). First, global hypomethylation and dense hypermethylation of certain CpG islands are associated with aging, a major risk factor for atherosclerosis (14). Second, hyperhomocysteinemia and the subsequent decreased production or bioavailability of SAM is associated with an increased risk of cardiovascular disease (15). Accordingly, mice with genetically reduced levels of methylenetetrahydrofolate reductase, a key enzyme in the pathway generating ...

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“…Apolipoprotein A-I has been shown to associate to euchromatic DNA [28]. These findings prompted attempts to identify apolipoprotein A-I-binding DNA sequences by in-vitro oligonucleotide binding assays [29]. The study concluded that a CG-rich 17-nucleotide sequence binds apolipoprotein A-I with high affinity.…”

Section: Previous Evidence For Lipids and Lipoprotein Components As Nmentioning

confidence: 99%

Chromatin modification by lipids and lipoprotein components: an initiating event in atherogenesis?

Zaina

Døssing

Lindholm

et al. 2005

Current Opinion in Lipidology

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Tetrahydrocortisol–apolipoprotein A-I complex specifically interacts with eukaryotic DNA and GCC elements of genes

Cited by 11 publications

References 18 publications

Apolipoprotein B epitopes are present in nuclear preparations of human and mouse cells

Apolipoprotein B epitopes are present in nuclear preparations of human and mouse cells

DNA Methylation Polymorphisms Precede Any Histological Sign of Atherosclerosis in Mice Lacking Apolipoprotein E

Chromatin modification by lipids and lipoprotein components: an initiating event in atherogenesis?

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