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      The Key Role of DNA Methylation and Histone Acetylation in Epigenetics of Atherosclerosis

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          Abstract

          Atherosclerosis, which is the most common chronic disease of the coronary artery, constitutes a vascular pathology induced by inflammation and plaque accumulation within arterial vessel walls. Both DNA methylation and histone modifications are epigenetic changes relevant for atherosclerosis. Recent studies have shown that the DNA methylation and histone modification systems are closely interrelated and mechanically dependent on each other. Herein, we explore the functional linkage between these systems, with a particular emphasis on several recent findings suggesting that histone acetylation can help in targeting DNA methylation and that DNA methylation may control gene expression during atherosclerosis.

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          TET enzymes, TDG and the dynamics of DNA demethylation.

          Rahul M. Kohli, Yi Zhang (2013)
          DNA methylation has a profound impact on genome stability, transcription and development. Although enzymes that catalyse DNA methylation have been well characterized, those that are involved in methyl group removal have remained elusive, until recently. The transformative discovery that ten-eleven translocation (TET) family enzymes can oxidize 5-methylcytosine has greatly advanced our understanding of DNA demethylation. 5-Hydroxymethylcytosine is a key nexus in demethylation that can either be passively depleted through DNA replication or actively reverted to cytosine through iterative oxidation and thymine DNA glycosylase (TDG)-mediated base excision repair. Methylation, oxidation and repair now offer a model for a complete cycle of dynamic cytosine modification, with mounting evidence for its significance in the biological processes known to involve active demethylation.
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            Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme.

            M Muramatsu, K Kinoshita, S Fagarasan … (2000)
            Induced overexpression of AID in CH12F3-2 B lymphoma cells augmented class switching from IgM to IgA without cytokine stimulation. AID deficiency caused a complete defect in class switching and showed a hyper-IgM phenotype with enlarged germinal centers containing strongly activated B cells before or after immunization. AID-/- spleen cells stimulated in vitro with LPS and cytokines failed to undergo class switch recombination although they expressed germline transcripts. Immunization of AID-/- chimera with 4-hydroxy-3-nitrophenylacetyl (NP) chicken gamma-globulin induced neither accumulation of mutations in the NP-specific variable region gene nor class switching. These results suggest that AID may be involved in regulation or catalysis of the DNA modification step of both class switching and somatic hypermutation.
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              Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques.

              Z. Galis, G Sukhova, M Lark … (1994)
              Dysregulated extracellular matrix (ECM) metabolism may contribute to vascular remodeling during the development and complication of human atherosclerotic lesions. We investigated the expression of matrix metalloproteinases (MMPs), a family of enzymes that degrade ECM components in human atherosclerotic plaques (n = 30) and in uninvolved arterial specimens (n = 11). We studied members of all three MMP classes (interstitial collagenase, MMP-1; gelatinases, MMP-2 and MMP-9; and stromelysin, MMP-3) and their endogenous inhibitors (TIMPs 1 and 2) by immunocytochemistry, zymography, and immunoprecipitation. Normal arteries stained uniformly for 72-kD gelatinase and TIMPs. In contrast, plaques' shoulders and regions of foam cell accumulation displayed locally increased expression of 92-kD gelatinase, stromelysin, and interstitial collagenase. However, the mere presence of MMP does not establish their catalytic capacity, as the zymogens lack activity, and TIMPs may block activated MMPs. All plaque extracts contained activated forms of gelatinases determined zymographically and by degradation of 3H-collagen type IV. To test directly whether atheromata actually contain active matrix-degrading enzymes in situ, we devised a method which allows the detection and microscopic localization of MMP enzymatic activity directly in tissue sections. In situ zymography revealed gelatinolytic and caseinolytic activity in frozen sections of atherosclerotic but not of uninvolved arterial tissues. The MMP inhibitors, EDTA and 1,10-phenanthroline, as well as recombinant TIMP-1, reduced these activities which colocalized with regions of increased immunoreactive MMP expression, i.e., the shoulders, core, and microvasculature of the plaques. Focal overexpression of activated MMP may promote destabilization and complication of atherosclerotic plaques and provide novel targets for therapeutic intervention.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Lipid Atheroscler
                Journal ID (publisher-id): JLA
                Title: Journal of Lipid and Atherosclerosis
                Publisher: Korean Society of Lipidology and Atherosclerosis
                ISSN (Print): 2287-2892
                ISSN (Electronic): 2288-2561
                Publication date (Print): September 2020
                Publication date (Electronic): 21 September 2020
                Volume: 9
                Issue: 3
                Pages: 419-434
                Affiliations
                [1 ]Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science, Seoul National University, Seoul, Korea.
                [2 ]Interdisciplinary Program in Stem Cell Biology, Graduate School of Medicine, Seoul National University, Seoul, Korea.
                [3 ]Department of Orthopedic Surgery, Seoul National University Hospital, Seoul, Korea.
                [4 ]Strategic Center of Cell and Bio Therapy for Heart, Diabetes & Cancer, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea.
                [5 ]Department of Medicine, College of Medicine, Seoul National University, Seoul, Korea.
                Author notes
                Correspondence to Yoo-Wook Kwon. Biomedical Research Institute, Seoul National University Hospital, 103 Daehak-ro, Jongno-gu, Seoul 03080, Korea. ywkwon@ 123456snu.ac.kr

                *Han-Teo Lee, Sanghyeon Oh and Du Hyun Ro contributed equally to this work.

                Author information
                https://orcid.org/0000-0003-1840-6749
                https://orcid.org/0000-0003-4770-6900
                https://orcid.org/0000-0001-6199-908X
                https://orcid.org/0000-0002-4752-5010
                https://orcid.org/0000-0003-2418-429X
                Article
                DOI: 10.12997/jla.2020.9.3.419
                PMC ID: 7521974
                PubMed ID: 33024734
                SO-VID: 17d860b5-b556-47e5-a09d-d6970fd0f2e9
                Copyright © Copyright © 2020 The Korean Society of Lipid and Atherosclerosis.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 08 May 2020
                Date revision received : 14 September 2020
                Date accepted : 15 September 2020
                Funding
                Funded by: Seoul National University Hospital, CrossRef https://doi.org/10.13039/501100004332;
                Award ID: 03-2017-0390
                Categories
                Subject: Review

                Keywords: dna methylation,histones,acetylation,atherosclerosis
                Data availability:
                Keywords: dna methylation, histones, acetylation, atherosclerosis

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