Aberrant DNA methylation of M1-macrophage genes in coronary artery disease

Bakshi, Chetan; Vijayvergiya, Rajesh; Dhawan, Veena

doi:10.1038/s41598-018-38040-1

Cited by 25 publications

(18 citation statements)

References 62 publications

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“…Previous studies have shown that abnormal DNA methylation in gene promoter regions is commonly related to AS [16–20]. Bakshi et al showed that the methylation levels of STAT1, IL12b, MHC2, iNOS, JAK1, and JAK2 were higher in coronary artery disease (CAD) patients than in control subjects [21]. Another study showed increased levels of the DNA demethylase TET1 and decreased levels of DNMT1 in atherosclerotic plaques [22].…”

Section: Introductionmentioning

confidence: 99%

miR-221 Alleviates the Ox-LDL-Induced Macrophage Inflammatory Response via the Inhibition of DNMT3b-Mediated NCoR Promoter Methylation

Guo³

et al. 2019

Mediators of Inflammation

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Atherosclerosis (AS) is a chronic inflammatory disease, and macrophages play a key role in all phases of AS. Recent studies have shown that miR-221 is a biomarker for AS and stroke; however, the role and mechanism of miR-221 in AS are unclear. Herein, we found that miR-221 and NCoR levels were decreased in ox-LDL-treated THP-1-derived macrophages. In contrast, DNMT3b, IL-6, and TNF-α expression levels were increased under these conditions. Upregulation of miR-221 or NCoR could partially inhibit ox-LDL-induced IL-6 and TNF-α expression. Further studies showed that DNMT3b was a target of miR-221. DNMT3b inhibition also suppressed IL-6 and TNF-α expression and increased NCoR expression in the presence of ox-LDL. Moreover, DNMT3b was involved in ox-LDL-induced DNA methylation in the promoter region of NCoR. These findings suggest that miR-221 suppresses ox-LDL-induced inflammatory responses via suppressing DNMT3b-mediated DNA methylation in the promoter region of NCoR. These results provide a rationale for using intracellular miR-211 as a possible antiatherosclerotic target.

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Section: Introductionmentioning

confidence: 99%

miR-221 Alleviates the Ox-LDL-Induced Macrophage Inflammatory Response via the Inhibition of DNMT3b-Mediated NCoR Promoter Methylation

Guo³

et al. 2019

Mediators of Inflammation

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“…Changes in DNA methylation have been associated with the biological and pathophysiological mechanisms of CVD (100)(101)(102)(103)(104)(105)(106)(107)(108)(109). Frequently, studies show an association of DNA methylation of repetitive sequences such as LINE1 (>500,000 copies, accounting for about 20% of the genome (109) with various types of CVD (100,(102)(103)(104)110).…”

Section: Epigenomicsmentioning

confidence: 99%

“…With advances in technologies for DNA methylation profiling, molecular epidemiologic studies show an association of genomewide DNA methylation alterations with CVD (103,(105)(106)(107)(108). A meta-analysis from 11,461 individuals identified seven differentially-methylated CpGs, annotated to DTX3L-PARP3, NLRC5, and ABO (105).…”

Section: Epigenomicsmentioning

confidence: 99%

“…Further, these studies found a causal impact of SLC1A5's methylation on CVD ( 106 ). Gene-specific promoter DNA methylation was altered in the blood of patients with coronary artery disease, the most common CVD ( 107 ), compared to controls. Another recent study identified over 60,000 CpGs to be differential methylation in ischemic from non-ischemic cardiomyopathy ( 108 ).…”

Section: Developments In the Fieldmentioning

confidence: 99%

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Use of an Exposome Approach to Understand the Effects of Exposures From the Natural, Built, and Social Environments on Cardio-Vascular Disease Onset, Progression, and Outcomes

Juárez

Hood

Song

et al. 2020

Front. Public Health

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Obesity, diabetes, and hypertension have increased by epidemic proportions in recent years among African Americans in comparison to Whites resulting in significant adverse cardiovascular disease (CVD) disparities. Today, African Americans are 30% more likely to die of heart disease than Whites and twice as likely to have a stroke. The causes of these disparities are not yet well-understood. Improved methods for identifying underlying risk factors is a critical first step toward reducing Black:White CVD disparities. This article will focus on environmental exposures in the external environment and how they can lead to changes at the cellular, molecular, and organ level to increase the personal risk for CVD and lead to population level CVD racial disparities. The external environment is defined in three broad domains: natural (air, water, land), built (places you live, work, and play) and social (social, demographic, economic, and political). We will describe how environmental exposures in the natural, built, and social environments "get under the skin" to affect gene expression though epigenetic, pan-omics, and related mechanisms that lead to increased risk for adverse CVD health outcomes and population level disparities. We also will examine the important role of metabolomics, proteomics, transcriptomics, genomics, and epigenomics in understanding how exposures in the natural, built, and social environments lead to CVD disparities with implications for clinical, public health, and policy interventions. In this review, we apply an exposome approach to Black:White CVD racial disparities. The exposome is a measure of all the exposures of an individual across the life course and the relationship of those exposures to health effects. The exposome represents the totality of exogenous (external) and endogenous (internal) exposures from conception onwards, simultaneously distinguishing, characterizing, and quantifying etiologic, mediating, moderating, and co-occurring risk and protective factors and their relationship to disease. Specifically, it assesses the biological mechanisms and underlying pathways through which chemical and non-chemical environmental Juarez et al. The Exposome and Cardiovascular Disease exposures are associated with CVD onset, progression and outcomes. The exposome is a promising approach for understanding the complex relationships among environment, behavior, biology, genetics, and disease phenotypes that underlie population level, Black: White CVD disparities.

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“…The evidence mentioned above reveals that aberrant DNA methylation modification exists in aging-related vascular diseases and might be a potential biomarker for the diagnosis and prognosis of vascular aging-related diseases ( Liu and Tang, 2019 ). Gene at DNA methylation status based on monocyte/macrophage might work as a diagnostic biomarker for clinical application ( Bakshi et al, 2019 ). Notably, hyperhomocysteine is associated with CVD, potentially influencing DNA methylation modification, suggesting that DNA methylation is a biomarker for the increased risk of CVD ( Kim et al, 2010 ).…”

Section: Dna Methylation As a Diagnostic Tool And Therapeutic Target In Vascular Aging-related Diseasesmentioning

confidence: 99%

Roles and Mechanisms of DNA Methylation in Vascular Aging and Related Diseases

Liu

2021

Front. Cell Dev. Biol.

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Vascular aging is a pivotal risk factor promoting vascular dysfunction, the development and progression of vascular aging-related diseases. The structure and function of endothelial cells (ECs), vascular smooth muscle cells (VSMCs), fibroblasts, and macrophages are disrupted during the aging process, causing vascular cell senescence as well as vascular dysfunction. DNA methylation, an epigenetic mechanism, involves the alteration of gene transcription without changing the DNA sequence. It is a dynamically reversible process modulated by methyltransferases and demethyltransferases. Emerging evidence reveals that DNA methylation is implicated in the vascular aging process and plays a central role in regulating vascular aging-related diseases. In this review, we seek to clarify the mechanisms of DNA methylation in modulating ECs, VSMCs, fibroblasts, and macrophages functions and primarily focus on the connection between DNA methylation and vascular aging-related diseases. Therefore, we represent many vascular aging-related genes which are modulated by DNA methylation. Besides, we concentrate on the potential clinical application of DNA methylation to serve as a reliable diagnostic tool and DNA methylation-based therapeutic drugs for vascular aging-related diseases.

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Aberrant DNA methylation of M1-macrophage genes in coronary artery disease

Cited by 25 publications

References 62 publications

miR-221 Alleviates the Ox-LDL-Induced Macrophage Inflammatory Response via the Inhibition of DNMT3b-Mediated NCoR Promoter Methylation

miR-221 Alleviates the Ox-LDL-Induced Macrophage Inflammatory Response via the Inhibition of DNMT3b-Mediated NCoR Promoter Methylation

Use of an Exposome Approach to Understand the Effects of Exposures From the Natural, Built, and Social Environments on Cardio-Vascular Disease Onset, Progression, and Outcomes

Roles and Mechanisms of DNA Methylation in Vascular Aging and Related Diseases

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