Methylation of FOXP3 in regulatory T cells is related to the severity of coronary artery disease

Jia, Lei; Zhu, Ling; Wang, Ji Zheng; Wang, Xiao Jian; Chen, Jing Zhou; Song, Lei; Wu, Yongjian; Sun, Kai; Yuan, Zuyi; Hui, Rutai

doi:10.1016/j.atherosclerosis.2013.01.027

Cited by 70 publications

(62 citation statements)

References 38 publications

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“…Regulation by DNA methylation also occurs in the promoter of FOXP3, the main transcription factor of the Treg cells that controls CD4 + -Th1/Th2 differentiation, thus playing a protective role in experimental atherosclerosis [80]. The FOXP3 promoter showed a difference in methylation levels between Treg and non-Treg CD4 + cells.…”

Section: Dna Methylation Modificationsmentioning

confidence: 98%

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Epigenetic Reprogramming in Atherosclerosis

Grimaldi

Vietri

Schiano

et al. 2014

Curr Atheroscler Rep

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Recent data support the involvement of epigenetic alterations in the pathogenesis of atherosclerosis. The most widely investigated epigenetic mechanism is DNA methylation although also histone code changes occur during the diverse steps of atherosclerosis, such as endothelial cell proliferation, vascular smooth muscle cell (SMC) differentiation, and inflammatory pathway activation. In this review, we focus on the main genes that are epigenetically modified during the atherogenic process, particularly nitric oxide synthase (NOS), estrogen receptors (ERs), collagen type XV alpha 1 (COL15A1), vascular endothelial growth factor receptor (VEGFR), and ten-eleven translocation (TET), which are involved in endothelial dysfunction; gamma interferon (IFN-γ), forkhead box p3 (FOXP3), and tumor necrosis factor-α (TNF-α), associated with atherosclerotic inflammatory process; and p66shc, lectin-like oxLDL receptor (LOX1), and apolipoprotein E (APOE) genes, which are regulated by high cholesterol and homocysteine (Hcy) levels. Furthermore, we also discuss the role of non-coding RNAs (ncRNA) in atherosclerosis. NcRNAs are involved in epigenetic regulation of endothelial function, SMC proliferation, cholesterol synthesis, lipid metabolism, and inflammatory response.

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Section: Dna Methylation Modificationsmentioning

confidence: 98%

“…In vitro analyses showed that oxLDL inhibited FOXP3 expression by upregulation of DNMT activity and subsequent DNA hypermethylation. Thus, Treg cells might play an important protective role in human ACS, downregulating Treg cells and in turn increasing the risk of atherosclerosis [80].…”

Section: Dna Methylation Modificationsmentioning

confidence: 99%

Epigenetic Reprogramming in Atherosclerosis

Grimaldi

Vietri

Schiano

et al. 2014

Curr Atheroscler Rep

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“…The first identifies an association between differential methylation at critical loci in lipoprotein metabolism (CETP, LPL) and a variety of metabolic abnormalities including HDL cholesterol and HDL particle size in familial hypercholesterolemia patients, by a candidate gene approach [26]. The other two reports describe DNAm markers of regulatory T-cell (Treg) function, a protective cell-type in atherosclerosis [27,28]. Because of its role in Treg activation, FOXP3 is the focus of both of the studies, in particular, a hypomethylated region of FOXP3 that is essential for Treg function.…”

Section: Search For Hematic Epigenetic Markers Of Atherosclerosismentioning

confidence: 97%

Unraveling the DNA methylome of atherosclerosis

Zaina

2014

Current Opinion in Lipidology

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“…DNA methylation was also implicated in the reduced autophagy of THP-1 macrophages upon exposure to oxidized LDL (oxLDL) [259]. Additionally, it was shown that oxLDL-induced epigenetic suppression of FOXP3 down-regulated T regulatory cells, subsequently increasing the risk of acute coronary syndrome [260]. OxLDL raised significantly MMP-2/MMP-9-mediated migration of human aortic SMCs by epigenetic effects mediated by miRNA [261].…”

Section: Histone Deacetylasesmentioning

confidence: 98%

Enzymatic Targets in Atherosclerosis

Fuior¹,

Trusca²,

Roman³

et al. 2015

J Mol Genet Med

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Atherosclerosis, a prime cause of mortality across the developed societies, was targeted by diverse therapeutic strategies. These evolved in response to the complex etiology and evolution of the disease. Many enzymes are associated with atherosclerosis, either in the main stream of lipid biosynthesis and transport or in the collateral and intertwined pathways of oxidative stress, inflammation, vascular remodeling or chromatin stability and are therefore revised herein. Enzyme exploration led to important developments. At the beginning, there were the statins, derived as inhibitors of hydroxy-methyl-glutaryl CoA (HMG-CoA) reductase, currently used widely to decrease lipid levels. At the other end, the inhibitors of the recently discovered proprotein convertase subtilisin/kexin type 9 (PCSK9) are awaiting the validation in clinical trials with great hopes for the future. In between, one can find some palliatives, as aspirin, an inhibitor of cyclooxygenase (COX), but also many invalidated candidates. Classical pharmacological data and newer approaches, like genetic knockouts in murine atherosclerosis models, are reviewed in order to appreciate the involvement of a particular enzyme in atherogenesis. However, the pursuit of an efficacious drug has been long and, in many cases, disappointing. Conclusions can be drawn from the overview of both successes and failures, in a quest for the best.

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Methylation of FOXP3 in regulatory T cells is related to the severity of coronary artery disease

Cited by 70 publications

References 38 publications

Epigenetic Reprogramming in Atherosclerosis

Epigenetic Reprogramming in Atherosclerosis

Unraveling the DNA methylome of atherosclerosis

Enzymatic Targets in Atherosclerosis

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