• Title/Summary/Keyword: Epigenetic

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Epigenetic Mechanisms of Depression: Role of Histone Modification and DNA Methylation in BDNF Gene (우울증의 후성유전기전: BDNF 유전자의 히스톤 변형 및 DNA 메틸화의 역할)

  • Park, Sung Woo
    • Journal of Life Science
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    • v.28 no.12
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    • pp.1536-1544
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    • 2018
  • Depression is a common, serious, and recurring mental disorder. The pathogenesis of depression involves many factors such as environmental factor, genetic factor and alteration of structure and function in neurobiological systems. Increasing evidence supports that epigenetic alteration may be associated with depression. The epigenetics is explained as the mechanisms by which environmental factor causes changes in chromatin structure and alters gene expression without changing DNA base sequence. DNA methylation and histone modification involving histone acetylation and methylation are the main epigenetic mechanisms. Animal studies have shown that stressful environment such as early life stress can leave persistent epigenetic marks in the genome, which alter gene expression and influence neural and behavioral function through adulthood. A potentially important gene in depression is brain-derived neurotrophic factor (BDNF). BDNF plays a central role in depression and antidepressant action. In studies of the rodent, exposure to stress at prenatal, postnatal, and adult stages alters BDNF expression through histone modification and DNA methylation of the BDNF gene which results in anxiety and depressive-like behavior. This review discusses recent advances in the study of the epigenetic mechanisms that contribute to depression, particularly histone modification and DNA methylation of the BDNF gene, that may help in the development of new targets for depression treatment.

Genetics of Prader-Willi Syndrome

  • Yoon, Ju Young
    • Journal of Interdisciplinary Genomics
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    • v.3 no.2
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    • pp.35-40
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    • 2021
  • Prader-Willi syndrome (PWS) is a rare genetic disorder which lead to severe neurodevelopmental, endocrine, and metabolic impairment. PWS is genetic disorder related to genomic errors which lead to inactivation of paternally-inherited genes on chromosome 15q11-q13. Epigenetic mechanisms are also involved in PWS, and epigenetic therapies are under investigation. Here we provide review about genetics of PWS, focused on genes involved in pathophysiology of PWS. We will also summarize epigenetics and genetic counseling of PWS.

Epigenetic aspects of telomeric chromatin in Arabidopsis thaliana

  • Lee, Won Kyung;Cho, Myeon Haeng
    • BMB Reports
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    • v.52 no.3
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    • pp.175-180
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    • 2019
  • Telomeres are nucleoprotein complexes at the physical ends of linear eukaryotic chromosomes. They protect the chromosome ends from various external attacks to avoid the loss of genetic information. Telomeres are maintained by cellular activities associated with telomerase and telomere-binding proteins. In addition, epigenetic regulators have pivotal roles in controlling the chromatin state at telomeres and subtelomeric regions, contributing to the maintenance of chromosomal homeostasis in yeast, animals, and plants. Here, we review the recent findings on chromatin modifications possibly associated with the dynamic states of telomeres in Arabidopsis thaliana.

Recovery of Genes Epigenetically Altered by the Histone Deacetylase Inhibitor Scriptaid and Demethylating Agent 5-Azacytidine in Human Leukemia Cells

  • Park, Eun-Kyung;Jeon, Eun-Hyung;Kim, In-Ho;Park, Seon-Yang
    • Genomics & Informatics
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    • v.8 no.4
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    • pp.185-193
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    • 2010
  • Histone deacetylation and demethylation are epigenetic mechanisms implicated in cancer. Studies regarding the role of modulation of gene expression utilizing the histone deacetylase inhibitor scriptaid and the demethylating agent 5-azacytidine in HL-60 leukemia cells have been limited. We studied the possibility of recovering epigenetically silenced genes by scriptaid and 5-azacytidine in human leukemia cells by DNA microarray analysis. The first group was leukemia cells that were cultured with 5-azacytidine. The second group was cultured with scriptaid. The other group was cultured with both agents. Two hundred seventy newly developed genes were expressed after the combination of 5-azacytidine and scriptaid. Twenty-nine genes were unchanged after the combination treatment of 5-azacytidine and scriptaid. Among the 270 genes, 13 genes were differed significantly from the control. HPGD, CPA3, CEACAM6, LOC653907, ETS1, RAB37, PMP22, FST, FOXC1, and CCL2 were up-regulated, and IGLL3, IGLL1, and ASS1 were down-regulated. Eleven genes associated with oncogenesis were found among the differentially expressed genes: ETS1, ASCL2, BTG2, BTG1, SLAMF6, CDKN2D, RRAS, RET, GIPC1, MAGEB, and RGL4. We report the results of our leukemia cell microarray profiles after epigenetic combination therapy with the hope that they are the starting point of selectively targeted epigenetic therapy.

Pre-Natal Epigenetic Influences on Acute and Chronic Diseases Later in Life, such as Cancer: Global Health Crises Resulting from a Collision of Biological and Cultural Evolution

  • Trosko, James E.
    • Preventive Nutrition and Food Science
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    • v.16 no.4
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    • pp.394-407
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    • 2011
  • Better understanding of the complex factors leading to human diseases will be necessary for both long term prevention and for managing short and long-term health problems. The underlying causes, leading to a global health crisis in both acute and chronic diseases, include finite global health care resources for sustained healthy human survival, the population explosion, increased environmental pollution, decreased clean air, water, food distribution, diminishing opportunities for human self-esteem, increased median life span, and the interconnection of infectious and chronic diseases. The transition of our pre-human nutritional requirements for survival to our current culturally-shaped diet has created a biologically-mismatched human dietary experience. While individual genetic, gender, and developmental stage factors contribute to human diseases, various environmental and culturally-determined factors are now contributing to both acute and chronic diseases. The transition from the hunter-gatherer to an agricultural-dependent human being has brought about a global crisis in human health. Initially, early humans ate seasonally-dependent and calorically-restricted foods, during the day, in a "feast or famine" manner. Today, modern humans eat diets of caloric abundance, at all times of the day, with foods of all seasons and from all parts of the world, that have been processed and which have been contaminated by all kinds of factors. No longer can one view, as distinct, infectious agent-related human acute diseases from chronic diseases. Moreover, while dietary and environmental chemicals could, in principle, cause disease pathogenesis by mutagenic and cytotoxic mechanisms, the primary cause is via "epigenetic", or altered gene expression, modifications in the three types of cells (e.g., adult stem; progenitor and terminally-differentiated cells of each organ) during all stages of human development. Even more significantly, alteration in the quantity of adult stem cells during early development by epigenetic chemicals could either increase or decrease the risk to various stem cell-based diseases, such as cancer, later in life. A new concept, the Barker hypothesis, has emerged that indicates pre-natal maternal dietary exposures can now affect diseases later in life. Examples from the studies of the atomic bomb survivors should illustrate this insight.

5-Aza-2'-deoxycytidine Induces Hepatoma Cell Apoptosis via Enhancing Methionine Adenosyltransferase 1A Expression and Inducing S-Adenosylmethionine Production

  • Liu, Wei-Jun;Ren, Jian-Guo;Li, Ting;Yu, Guo-Zheng;Zhang, Jin;Li, Chang-Sheng;Liu, Zhi-Su;Liu, Quan-Yan
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.11
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    • pp.6433-6438
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    • 2013
  • In hepatocellular cancer (HCC), lack of response to chemotherapy and radiation treatment can be caused by a loss of epigenetic modifications of cancer cells. Methionine adenosyltransferase 1A is inactivated in HCC and may be stimulated by an epigenetic change involving promoter hypermethylation. Therefore, drugs releasing epigenetic repression have been proposed to reverse this process. We studied the effect of the demethylating reagent 5-aza-2'-deoxycitidine (5-Aza-CdR) on MAT1A gene expression, DNA methylation and S-adenosylmethionine (SAMe) production in the HCC cell line Huh7. We found that MAT1A mRNA and protein expression were activated in Huh7 cells with the treatment of 5-Aza-CdR; the status of promoter hypermethylation was reversed. At the same time, MAT2A mRNA and protein expression was significantly reduced in Huh7 cells treated with 5-Aza-CdR, while SAMe production was significantly induced. However, 5-Aza-CdR showed no effects on MAT2A methylation. Furthermore, 5-Aza-CdR inhibited the growth of Huh7 cells and induced apoptosis and through down-regulation of Bcl-2, up-regulation of Bax and caspase-3. Our observations suggest that 5-Aza-CdR exerts its anti-tumor effects in Huh7 cells through an epigenetic change involving increased expression of the methionine adenosyltransferase 1A gene and induction of S-adenosylmethionine production.

Epigenetic modification of retinoic acid-treated human embryonic stem cells

  • Cheong, Hyun-Sub;Lee, Han-Chul;Park, Byung-Lae;Kim, Hye-Min;Jang, Mi-Jin;Han, Yong-Mahn;Kim, Seun-Young;Kim, Yong-Sung;Shin, Hyoung-Doo
    • BMB Reports
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    • v.43 no.12
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    • pp.830-835
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    • 2010
  • Epigenetic modification of the genome through DNA methylation is the key to maintaining the differentiated state of human embryonic stem cells (hESCs), and it must be reset during differentiation by retinoic acid (RA) treatment. A genome-wide methylation/gene expression assay was performed in order to identify epigenetic modifications of RA-treated hESCs. Between undifferentiated and RA-treated hESCs, 166 differentially methylated CpG sites and 2,013 differentially expressed genes were discovered. Combined analysis of methylation and expression data revealed that 19 genes (STAP2, VAMP8, C10orf26, WFIKKN1, ELF3, C1QTNF6, C10orf10, MRGPRF, ARSE, LSAMP, CENTD3, LDB2, POU5F1, GSPT2, THY1, ZNF574, MSX1, SCMH1, and RARB) were highly correlated with each other. The results provided in this study will facilitate future investigations into the interplay between DNA methylation and gene expression through further functional and biological studies.