• Molecules and Cells
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• v.41 no.4
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• pp.264-270
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• 2018

Cells cope with diverse intrinsic and extrinsic stimuli in order to make adaptations for survival. The epigenetic landscape plays a crucial role in cellular adaptation, as it integrates the information generated from stimuli. Signaling pathways induced by stimuli communicate with chromatin to change the epigenetic landscape through regulation of epigenetic modifiers. Metabolic dynamics altered by these stimuli also affect the activity of epigenetic modifiers. Here, I review the current understanding of epigenetic regulation via signaling and metabolic pathways. In addition, I will discuss possible ways to achieve specificity of epigenetic modifications through the cooperation of stimuli-induced signal transduction and metabolic reprogramming.

• BMB Reports
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• v.49 no.12
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• pp.671-680
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• 2016

Accumulating evidence indicates many brain functions are mediated by epigenetic regulation of neural genes, and their dysregulations result in neuronal disorders. Experiences such as learning and recall, as well as physical exercise, induce neuronal activation through epigenetic modifications and by changing the noncoding RNA profiles. Animal models, brain samples from patients, and the development of diverse analytical methods have broadened our understanding of epigenetic regulation in the brain. Diverse and specific epigenetic changes are suggested to correlate with neuronal development, learning and memory, aging and age-related neuronal diseases. Although the results show some discrepancies, a careful comparison of the data (including methods, regions and conditions examined) would clarify the problems confronted in understanding epigenetic regulation in the brain.

• Toxicological Research
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• v.31 no.1
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• pp.1-9
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• 2015

Environmental toxicants such as toxic metals can alter epigenetic regulatory features such as DNA methylation, histone modification, and non-coding RNA expression. Heavy metals influence gene expression by epigenetic mechanisms and by directly binding to various metal response elements in the target gene promoters. Given the role of epigenetic alterations in regulating genes, there is potential for the integration of toxic metal-induced epigenetic alterations as informative factors in the risk assessment process. Here, we focus on recent advances in understanding epigenetic changes, gene expression, and biological effects induced by toxic metals.

• Molecules and Cells
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• v.38 no.8
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• pp.677-684
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• 2015

Osteoarthritis (OA) is one of the most prevalent forms of joint disorder, associated with a tremendous socioeconomic burden worldwide. Various non-genetic and lifestyle-related factors such as aging and obesity have been recognized as major risk factors for OA, underscoring the potential role for epigenetic regulation in the pathogenesis of the disease. OA-associated epigenetic aberrations have been noted at the level of DNA methylation and histone modification in chondrocytes. These epigenetic regulations are implicated in driving an imbalance between the expression of catabolic and anabolic factors, leading eventually to osteoarthritic cartilage destruction. Cellular senescence and metabolic abnormalities driven by OA-associated risk factors appear to accompany epigenetic drifts in chondrocytes. Notably, molecular events associated with metabolic disorders influence epigenetic regulation in chondrocytes, supporting the notion that OA is a metabolic disease. Here, we review accumulating evidence supporting a role for epigenetics in the regulation of cartilage homeostasis and OA pathogenesis.

• Preventive Nutrition and Food Science
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• v.22 no.2
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• pp.81-89
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• 2017

Healthy aging has become a major goal of public health. Many studies have provided evidence and theories to explain molecular mechanisms of the aging process. Recent studies suggest that epigenetic mechanisms are responsible for life span and the progression of aging. Epigenetics is a fascinating field of molecular biology, which studies heritable modifications of DNA and histones that regulate gene expression without altering the DNA sequence. DNA methylation is a major epigenetic mark that shows progressive changes during aging. Recent studies have investigated aging-related DNA methylation as a biomarker that predicts cellular age. Interestingly, growing evidence proposes that nutrients play a crucial role in the regulation of epigenetic modifiers. Because various nutrients and their metabolites function as substrates or cofactors for epigenetic modifiers, nutrition can modulate or reverse epigenetic marks in the genome as well as expression patterns. Here, we will review the results on aging-associated epigenetic modifications and the possible mechanisms by which nutrition, including nutrient availability and bioactive compounds, regulate epigenetic changes and affect aging physiology.

• The Journal of the Korea Contents Association
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• v.13 no.8
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• pp.466-473
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• 2013

Gene expression is regulated by a wide range of mechanisms at the DNA sequence level. In addition, gene expression is also regulated by epigenetic mechanisms through DNA methylation, histone modification, and ncRNA. To understand the regulation of gene expression at the epigenetic level, we constructed aging related gene database and analyzed epigenetic properties that are focused on DNA methylation. The DNA methylation of promoter or upstream region of the genes induces to repress the gene expression. We compared and analyzed distribution between whole human genes and aging related genes in the epigenetic properties such as CGI distribution, methylation motif pattern, and TFBS (transcription factor binding site) distribution. In contrast to methylation motif pattern, CGI and TFBS distributions are positively correlated with epigenetic regulation of aging related gene expression. In this study, the epigenetic data about DNA methylation of the aging genes will provide us to understand phenomena of the aging and epigenetic mechanism for regulation of aging related genes.

• Korean Journal of Plant Tissue Culture
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• v.27 no.5
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• pp.359-366
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• 2000

Epigenetics represents a chromatin-mediated transcriptional repression which plays a control role in both animal and plant development. A number of different mechanisms have been described to be involved in the formation of chromatin structure: especially DNA methylation, nucleosomal histone modification, DNA replication timing, and binding of chromatin remodelling proteins. Epigenetic phenomena include genomic imprinting, dosage compensation of X-chromosome linked genes, mutual allelic interactions, paramutation, transvection, silencing of invasive DNA sequences, etc. They are often unstable and inherited in a non-Mendelian way. A number of epigenetic defects has been preferentially described in floral development. Here, epigenetic phenomena in model angiosperm plants and their corresponding mechanisms are reviewed.

• Molecules and Cells
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• v.40 no.1
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• pp.10-16
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• 2017

When peripheral axons are damaged, neuronal injury signaling pathways induce transcriptional changes that support axon regeneration and consequent functional recovery. The recent development of bioinformatics techniques has allowed for the identification of many of the regeneration-associated genes that are regulated by neural injury, yet it remains unclear how global changes in transcriptome are coordinated. In this article, we review recent studies on the epigenetic mechanisms orchestrating changes in gene expression in response to nerve injury. We highlight the importance of epigenetic mechanisms in discriminating efficient axon regeneration in the peripheral nervous system and very limited axon regrowth in the central nervous system and discuss the therapeutic potential of targeting epigenetic regulators to improve neural recovery.

• Animal Bioscience
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• v.34 no.8
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• pp.1271-1282
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• 2021

Genome-wide studies provide considerable insights into the genetic background of animals; however, the inheritance of several heritable factors cannot be elucidated. Epigenetics explains these heritabilities, including those of genes influenced by environmental factors. Knowledge of the mechanisms underlying epigenetics enables understanding the processes of gene regulation through interactions with the environment. Recently developed next-generation sequencing (NGS) technologies help understand the interactional changes in epigenetic mechanisms. There are large sets of NGS data available; however, the integrative data analysis approaches still have limitations with regard to reliably interpreting the epigenetic changes. This review focuses on the epigenetic mechanisms and profiling methods and multi-omics integration methods that can provide comprehensive biological insights in animal genetic studies.

• Molecules and Cells
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• v.39 no.11
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• pp.783-789
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• 2016

Afflicted neurons in various neurodegenerative diseases generally display diverse and complex pathological features before catastrophic occurrence of massive neuronal loss at the late stages of the diseases. This complex nature of neuronal pathophysiology inevitably implicates systemwide changes in basic cellular activities such as transcriptional controls and signal cascades, and so on, as a cause. Recently, as one of these systemwide cellular changes associated with neurodegenerative diseases, epigenetic changes caused by protein toxicity have begun to be highlighted. Notably, recent advances in related techniques including next-generation sequencing (NGS) and mass spectrometry enable us to monitor changes in the post-translational modifications (PTMs) of histone proteins and to link these changes in histone PTMs to the specific transcriptional changes. Indeed, epigenetic alterations and consequent changes in neuronal transcriptome are now begun to be extensively studied in neurodegenerative diseases including Alzheimer's disease (AD). In this review, we will discuss details of our current understandings on epigenetic changes associated with two representative neurodegenerative diseases [AD and polyglutamine (polyQ) diseases] and further discuss possible future development of pharmaceutical treatment of the diseases through modulating these epigenetic changes.