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Systemic Lupus Erythematosus
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Vaneet K. Sandhu, Neha V. Chiruvolu, Daniel J. Wallace
DNA methylation is an epigenetic mechanism where a methyl group is transferred to the fifth carbon of the cytosine pyrimidine ring and involved in cell differentiation, silencing of transposable elements, and gene imprinting. UV light, hydralazine, and procainamide can inhibit DNA methylation, inciting SLE-like disease. One of the first studies on DNA methylation showed that suppressing this process in CD4+ T cells during mitosis led to formation of autoreactive CD4+ T cells. This was backed by more studies which revealed that expression of genes suppressed by DNA methylation can lead to T cell–mediated autoreactivity.83 Studies with microarrays have shown that hypomethylation of IFN genes such as MX1, BST2, and IFI44L can lead to SLE pathogenesis.50
Genetics and exercise: an introduction
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Claude Bouchard, Henning Wackerhage
In summary, the profile of DNA methylation and chemical modification of histone proteins constitutes the epigenome. Epigenetic modifications can occur at all ages as a result of exposure to environmental factors, such as nutrients, cellular insults and stress. The research on whether acute exercise, exercise training or inactivity are stimuli that can trigger epigenetic events is discussed later in this book (Chapter 6). Retained epigenetic modifications to DNA in skeletal muscle tissue have been identified following exercise training, even after a period of detraining, and therefore a so-called epigenetic memory or “epi-memory” of prior exercise has been proposed. Epigenetics of exercise and muscle “memory” are also discussed in detail later in this book (Chapter 6).
Exercise, Metabolism and Oxidative Stress in the Epigenetic Landscape
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
Gareth W. Davison, Colum P. Walsh
DNA methylation occurs in two contexts aided by three DNA methyltransferase (DNMT) enzymes. DNMT1 is a maintenance methyltransferase, which recognises hemimethylated DNA to form a symmetrically modified duplex during DNA replication, while DNMT3A and DNMT3B are primarily de novo enzymes that deposit CH3 marks on previously unmodified cytosines (Okano et al., 1999; Grurnbaum et al., 1982). Methylation of DNA occurs with the addition of CH3 at the C5 position of the nucleoside cytosine, forming 5-methylcytosine (5mC) on CpG dinucleotides (80% of cytosine residues in CpG dinucleotides are methylated at position 5, Davison et al., 2021). The CpG dinucleotide is unique in that it only occurs at a low frequency, while simultaneously converging into CpG islands (CGI) extending for 300–3,000 base pairs, mainly in regulatory elements of genes such as enhancer and promoter regions (Hitchler and Domann, 2021). Located up- and downstream of CpG islands are CpG shores and CpG shelves which display greater tissue-specific methylation profiles (Seaborne and Sharples, 2020). Methylation is absent in CGI AT promoter regions with active transcription. However, when promoter-associated CGI are methylated, transcription is silenced (Bird, 2007). More recently, it has been shown by a number of genome-wide and functional studies that DNA methylation in the gene body also facilitates transcription (Wu et al., 2010; Neri et al., 2013; Irwin et al., 2014).
Targeted sequencing approach: Comprehensive analysis of DNA methylation and gene expression across blood and brain regions in suicide victims
Published in The World Journal of Biological Psychiatry, 2023
Katarina Kouter, Tomaž Zupanc, Alja Videtič Paska
DNA methylation is the addition of a single methyl group to a cytosine, leading to formation of 5-methylcytosine (5mC) (Prokhortchouk and Defossez 2008). The reaction is catalysed by enzymes from the DNA methyltransferases (DNMT) family, with the donor of methyl group being S-adenosyl methionine (Lyko 2018). 5mC can usually be found clustered in CpG dinucleotide motifs. CpG clusters form CpG islands (CGI) and act as regulators of gene expression in promoters and first exons (Deaton and Bird 2011). Methylation of a promotor CpG island is often associated with decreased levels of gene expression (Illingworth and Bird 2009). DNA methylation may affect gene expression following two mechanisms. First, addition of a methyl group alters DNA biophysical properties and prevents the binding of transcriptional factors to DNA (Lee et al. 2014). Second, it attracts proteins that bind to methylated DNA and thus prevent gene transcription (Du et al. 2015).
Association between the Extent of Peripheral Blood DNA Methylation of HIF3A and Accumulation of Adiposity in community-dwelling Women: The Yakumo Study
Published in Endocrine Research, 2022
Genki Mizuno, Hiroya Yamada, Eiji Munetsuna, Mirai Yamazaki, Yoshitaka Ando, Ryosuke Fujii, Yoshiki Tsuboi, Atsushi Teshigawara, Itsuki Kageyama, Keisuke Osakabe, Keiko Sugimoto, Hiroaki Ishikawa, Naohiro Ichino, Yoshiji Ohta, Koji Ohashi, Shuji Hashimoto, Koji Suzuki
Lifestyle and/or environmental factors cause epigenetic alterations, which play a critical role in several health conditions such as obesity and metabolic disease.13–16 DNA methylation is an epigenetic mechanism that regulates gene expression by adding a methyl donor to cytosine to enable the regulation of transcription.17 Lifestyle factors, including dietary habits, modulate DNA methylation.18,19 Several animal20–22 and epidemiological studies23–25 have shown that environmental factors, including food intake, tobacco smoking, and alcohol consumption, cause DNA methylation in blood or tissues. Moreover, global DNA hypermethylation of leukocytes is associated with an increased risk of cardiovascular diseases in the general Japanese population.26 Thus, DNA methylation might be a novel biomarker of metabolic diseases caused by environmental factors and lifestyle.
DNA methylation in pulmonary fibrosis and lung cancer
Published in Expert Review of Respiratory Medicine, 2022
Juan Duan, Baiyun Zhong, Zhihua Fan, Hao Zhang, Mengmeng Xu, Xiangyu Zhang, Yan Y Sanders
Lung cancer and fibrosis are two distinct diseases that share multiple cellular and molecular mechanisms, including alterations in DNA methylation. In this review, we focus on traditional DNA methylation, excluding other forms of DNA modification, such as the recently identified DNA hydroxymethylation, which shows its importance as an epigenetic regulator of gene expression. DNA methylation and demethylation play pivotal roles in lung cancer and fibrosis. DNA methylation at a gene’s regulatory region can either directly regulate gene expression or recruit MBPs to areas that affect related regulatory complexes, activating or repressing gene expression according to cellular cues. Alterations in methylation patterns can be used for diagnosis or therapeutic targets. Although epigenetic biomarkers reveal substantial potential for clinical application, these studies are still in their infancy. DNA methylation signatures are stable and relatively easy to detect in tissues and body fluids [89,90]. Establishing such markers would be invaluable for the early diagnosis and prognosis of lung cancer and lung fibrosis, which would also aid in predicting treatment efficacy and tracking treatment efficiency or resistance. Efforts to identify and establish methylation biomarkers using plasma cell-free DNA have been reported in both lung cancer and fibrosis, and were able to differentiate between lung cancer, pulmonary fibrosis, and healthy subjects [91]. However, transcriptome and methylation profiles of lung cancer in patients with IPF remain unclear.