June 20, 2021

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Epigenetic Regulation of Normal Human Mammary Cell Type Specific MiRNAs

Epigenetic Regulation of Normal Human Mammary Cell Type Specific MiRNAs
Author : Anonim
Publisher : Unknown
Release Date : 2011
Category :
Total pages :129
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Epigenetic mechanisms are important regulators of cell type-specific genes, including miRNAs. In order to identify cell type-specific miRNAs regulated by epigenetic mechanisms, we undertook a global analysis of miRNA expression and epigenetic states in three isogenic pairs of human mammary epithelial cells (HMEC) and human mammary fibroblasts (HMF), which represent two differentiated cell types typically present within a given organ, each with a distinct phenotype and a distinct epigenotype. While miRNA expression and epigenetic states showed strong interindividual concordance within a given cell type, almost 10% of the expressed miRNA showed a cell type-specific pattern of expression that was linked to the epigenetic state of their promoter. The tissue-specific miRNA genes were epigenetically repressed in nonexpressing cells by DNA methylation (38%) and H3K27me3 (58%), with only a small set of miRNAs (21%) showing a dual epigenetic repression where both DNA methylation and H3K27me3 were present at their promoters, such as MIR10A and MIR10B. Individual miRNA clusters of closely related miRNA gene families can each display cell type-specific repression by the same or complementary epigenetic mechanisms, such as the MIR200 family, and MIR205, where fibroblasts repress MIR200C/141 by DNA methylation, MIR200A/200B/429 by H3K27me3, and MIR205 by both DNA methylation and H3K27me3. Since deregulation of many of the epigenetically regulated miRNAs that we identified have been linked to disease processes such as cancer, it is predicted that compromise of the epigenetic control mechanisms is important for this process. Overall, these results highlight the importance of epigenetic regulation in the control of normal cell type-specific miRNA expression.

Epigenetic Regulation of MicroRNAs in Chronic Lymphocytic Leukemia

Epigenetic Regulation of MicroRNAs in Chronic Lymphocytic Leukemia
Author : Constance Regina Bär
Publisher : Unknown
Release Date : 2013
Category :
Total pages :130
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Epigenetic Regulation in the Nervous System

Epigenetic Regulation in the Nervous System
Author : Quan Lin,Yi E. Sun
Publisher : Elsevier Inc. Chapters
Release Date : 2012-12-31
Category : Medical
Total pages :374
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Epigenetics of Chronic Pain

Epigenetics of Chronic Pain
Author : Anonim
Publisher : Academic Press
Release Date : 2018-10-29
Category : Medical
Total pages :248
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Epigenetics of Chronic Pain, Volume Nine, presents comprehensive information on the role of epigenetics in chronic pain sensitivity, providing a detailed, but accessible, view of the field from basic principles, to clinical application. Leading international researchers discuss essential mechanisms of chronic pain epigenetics, including the molecular processes of chromatin remodeling, histone modifications, and the microRNAs and noncoding RNAs involved in regulating genes tied to pain sensitivity. The influence of epigenetics in inflammatory, neuropathic, visceral and other pain models is examined, with data derived from epigenetic studies on peripheral and central mechanisms of pain sensitivity in animal models and clinical cases studies. The studies and case examples cited highlight therapeutic pathways of significance and next steps for researchers to develop epigenetic-based treatments for chronic pain. In recent years, epigenetic regulation of gene expression has been shown to play a central role in managing human pain sensitivity. Findings show that expression of many genes critical to increases or decreases in pain sensitivity are indeed regulated by DNA methylation and its enzymes, histone-involved chromatin remodeling, and noncoding RNAs, mainly microRNAs. Compiles all known information on epigenetic regulation of chronic pain in one volume Covers the basic functionality of epigenetic mechanisms involved in pain management, applications of recent research in understanding different types of chronic pain, and pathways for developing therapeutics Leading international researchers from across academia, clinical settings, and the pharmaceutical industry discuss epigenetics in inflammatory, neuropathic, visceral, and other pain models in-depth Enables clinicians, researchers, and pharmacologists to better understand and treat chronic pain

Epigenetics of B Cells and Antibody Responses

Epigenetics of B Cells and Antibody Responses
Author : Paolo Casali
Publisher : Frontiers Media SA
Release Date : 2016-04-12
Category :
Total pages :129
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Epigenetics is the study of changes in gene activity that are heritable but not caused by changes in the DNA sequence. By modulating gene activities, epigenetic changes regulate cell functions. They include DNA methylation, histone posttranslational modifications and gene silencing by the action of non-coding RNAs, particularly microRNAs. It is now clear that epigenetic changes regulate B cell development. By acting in concert with networks of transcription factors, they modulate the activation of B cell lineage specific gene programs and repress inappropriate gene transcription in particular B cell differentiation states.

A hallmark of B cell development in the bone marrow is the assembly of the B cell receptor (BCR) for antigen through rearrangement of immunoglobulin heavy (IgH) and light (IgL) chain V(D)J genes, as mediated by RAG1/RAG2 recombinases. Ig V(D)J rearrangement critically times the progression from pro-B cell to pre-B cell and, finally, mature B cell. Such progression is modulated by epigenetic marks, such as DNA methylation and histone posttranslational modifications, that increase chromatin accessibility and target RAG/RAG2 to V, D and J DNA. It is also dependent on the expression of multiple microRNAs. Mice deficient in Ago2, which is essential for microRNA biogenesis and function, have B cell development blocked at the pro-B cell stage. In agreement with this, B cell specific ablation of microRNA by B cell-specific knockout of Dicer virtually blocks B cell differentiation at the pro-B to pre-B cell transition.

After mature B cells encounter antigen, changes of the epigenetic landscape are induced by the same stimuli that drive the antibody response; such epigenetic changes underpin the maturation of the antibody response itself. They instruct those B cell differentiation processes, somatic hypermutation (SHM), class switch DNA recombination (CSR) and plasma cell differentiation, that are central to the maturation of the antibody response as well as differentiation of memory B cells. Inducible histone modifications, together with DNA methylation and microRNAs modulate the transcriptome, particularly the expression of activation-induced cytidine deaminase (AID), central to SHM and CSR, and B lymphocyte-induced maturation protein-1 (Blimp-1), which is central to plasma cell differentiation.

Combinatorial histone modifications also function as histone codes in the targeting of the CSR and, possibly, the SHM machinery to the Ig locus by recruiting specific adaptors (histone code readers) that can in turn target and/or stabilize CSR/SHM factors. Epigenetic alterations in memory B cells contribute to their functionally distinction from their naive counterparts. Memory B cells inherit epigenetic information from their precursors and acquire new epigenetic marks, which make these resting B cells poised to promptly respond to antigen. The cross/feedback regulation of different epigenetic modifications/elements further increases the complexity of the B cell epigenome, which interacts with the genetic information for precise modulation of gene expression. It is increasingly evident that epigenetic dysregulation in B cells, including aberrant expression of microRNAs, can result in aberrant antibody responses to microbial pathogens, emergence of pathogenic autoantibodies or B cell neoplastic transformation. Epigenetic marks are potential targets for new therapeutics in autoimmunity and B cell malignancy.

Pitx2 Expression and Epigenetic Regulation of Muscle Cell Differentiation

Pitx2 Expression and Epigenetic Regulation of Muscle Cell Differentiation
Author : Jing Rong
Publisher : Unknown
Release Date : 2014
Category :
Total pages :206
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Epigenetic modifications are heritable, stable and potentially reversible changes in gene expression, and occur without change in DNA sequence. These changes may involve DNA methylation, histone acetylation, or regulation of non-coding RNAs such as microRNAs. The significance of epigenetic modifications has been highlighted in human diseases ranging from inherited cancer to muscular dystrophy. In our previous study, significant DNA methylation change of paired-like homedomain 2 (Pitx2) gene was found in human skeletal muscle of the kwashiorkor and marasmus survivors; three CpG sites on Pitx2 were differentially methylated. Therefore, this study explores the relationship between Pitx2 expression and epigenetic modifications, in particular DNA methylation and microRNA regulation, during myogenic differentiation by using the murine C2C12 myoblast cell line as an in vitro muscle cell model. It was found that Pitx2 expression change during myogenic differentiation in C2C12 myoblasts was not accompanied by the DNA methylation change in the three CpG sites of interest. In addition, following Pitx2 knock-down and myogenic differentiation in C2C12 myoblasts, two myogenic regulators Myf5 and Myogenin were up-regulated and microRNA miR-127 and miR-486 expression were significantly inhibited. In addition, miR-27a, miR-29b and miR-133a tended to decrease following Pitx2 knock-down. Overall data suggest that Pitx2 may participate in the myogenic regulatory network through regulating microRNA at least via miR-486. Furthermore, results from this study also suggest that Myogenin may be an important mediator in these regulatory pathways.

Epigenetic Regulation by MiRNA Derived from Pag-1 During HzNV-1 Infection

Epigenetic Regulation by MiRNA Derived from Pag-1 During HzNV-1 Infection
Author : 吳珮綺
Publisher : Unknown
Release Date : 2017
Category :
Total pages :129
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Epigenetics in Plants of Agronomic Importance: Fundamentals and Applications

Epigenetics in Plants of Agronomic Importance: Fundamentals and Applications
Author : Raúl Alvarez-Venegas,Clelia De-la-Peña,Juan Armando Casas-Mollano
Publisher : Springer
Release Date : 2019-04-26
Category : Science
Total pages :415
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Over the past few decades, chromatin modulation has emerged as an important regulator of gene expression. This second edition provides detailed information on the epigenetic mechanisms in plants, illustrating the value of this research in plants of agronomic importance. It examines recent advances regarding plants’ epigenetic regulation in response to abiotic and biotic types of stress; the epigenetic basis of plant immunity; evolution and functions of plant histones; epigenetic variation and plant breeding; and epigenome editing and crop improvement. The content is intended to promote the development of future biotechnologies to manipulate and selectively activate/inhibit proteins and metabolic pathways to counter pathogens, to treat important diseases, and to increase crop productivity. The development of new fields, like epigenome editing and RNA epigenetics, will certainly improve our understanding of currently known epigenetic modifications and their roles in e.g. host-pathogen interactions, crop productivity, and in response to environmental stimuli. This volume contains twelve new/revised chapters, written by an international team of experts on plant epigenetics, and addresses the needs of researchers and professionals in the fields of agronomics, crop breeding, epigenetics, plant biochemistry, plant developmental biology, and related disciplines.

Macro Roles for MicroRNAs in the Life and Death of Neurons

Macro Roles for MicroRNAs in the Life and Death of Neurons
Author : Bart De Strooper
Publisher : Springer Science & Business Media
Release Date : 2009-12-01
Category : Medical
Total pages :121
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The discovery of microRNAs has revealed an additional level of fine tuning of the genome and how genes are used again and again in different combinations to generate the complexity that underlies for instance the brain. This book examines this field.

miRNA and Cancer

miRNA and Cancer
Author : Anonim
Publisher : Academic Press
Release Date : 2017-09-04
Category : Science
Total pages :230
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miRNA and Cancer, Volume 135, the latest volume in the Advances in Cancer Research series, provides invaluable information on the exciting and fast-moving field of cancer research. This volume presents original reviews on research bridging oncology and gene expression, and includes specific chapters on Non-coding RNAs as Biomarkers of Cancer, The Enigma of microRNA Regulation in Cancer, Animal Models to Study microRNA functions, Non-coding RNAs and Cancer, microRNAs in Cancer Susceptibility, ts-RNAs versus microRNAs, microRNAs and AML, and microRNAs and Epigenetics. Provides information on cancer research Offers outstanding and original reviews on a range of cancer research topics Serves as an indispensable reference for researchers and students alike

Epigenetics and Cancer

Epigenetics and Cancer
Author : Fazlul H. Sarkar
Publisher : Springer Science & Business Media
Release Date : 2013-05-29
Category : Medical
Total pages :287
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Overall, this book illustrates the complexities of the regulation and deregulation of genes mediated through epigenetics in the development and progression of human malignancies. All the articles have been carefully chosen to represent several cancer systems with state of our knowledge on the role of epigenetic deregulation of microRNAs (miRNAs) and their target mRNAs along with epigenetic deregulation of mRNAs. This book also illustrates the role of several dietary agents, collectively called nutraceuticals or natural agents in modulating the epigenetic reprogramming of miRNAs and mRNAs for the prevention and/or treatment of human malignancies. It is well known that genetic aberrations, especially inherited through parents (somatic genetic alterations) contribute to the development of less than 10% of all cancer yet epigenetic alterations in genes especially through selective methylation and acetylation appears to be responsible for the development and progression of the vast majority of all cancers. Therefore, understanding the role of epigenetics in the regulation of genes especially through deregulated expression of miRNAs as presented in this book will allow scientists to devise targeted therapeutic strategies for re-expression of the lost genes or down-regulate the genes that are over-expressed in order to eradicate cancer. It is hoped that targeting epigenetics will not only target cancer cells but it will also target the tumor microenvironment (more like the entire tumor environment such as the entire host) for achieving better treatment outcomes for patients diagnosed with cancer which will lead to achieve the long-term objective for complete eradication of cancer. This book contains fifteen chapters which begins with the concept of systems and network biology for investigating the epigenetics of cancer followed by a series of articles on the role of miRNAs and their target genes in the biology of pancreatic cancer and other cancers such as breast, kidney, prostate and and colon. Since it is becoming increasingly clear that cancer stem cells (CSCs) are important in the development and progression of cancer, and CSCs are important in therapeutic resistance, treatment failure and tumor recurrence, thus the importance of CSCs and epigenetics has been highlighted by a very timely article on epigenetic variations of stem cell markers in cancer including miRNAs. Moreover, just targeting heterogeneous cancer cell populations may not be optimal to eradicate tumors and for which one must take a holistic approach for developing drugs that could also target the tumor microenvironment and tumor dormancy that are regulated through epigenetics. Keeping abreast with this thought process the concluding chapter provides a concept towards curative cancer therapy with maspin, which could be a unique window of opportunity to target tumor dormancy. Therefore, it suggest that targeting the tumor dormancy and the tumor microenvironment using novel therapeutics specifically by targeting epigenetics would become the future of medicine.

Improving Autophagy in Cystic Fibrosis

Improving Autophagy in Cystic Fibrosis
Author : Mia Farrah Tazi
Publisher : Unknown
Release Date : 2015
Category :
Total pages :120
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Cystic Fibrosis (CF) is a fatal, genetic disorder that critically affects the lungs and is directly caused by mutations in the CF transmembrane conductance regulator (CFTR) gene, resulting in defective CFTR protein function. Autophagy is a highly-regulated biological process that provides energy during periods of stress and starvation. Normally, it functions to clear pathogens and dysfunctional protein aggregates within macrophages. This process is impaired in CF patients and CF mice, as their macrophages exhibit limited autophagy activity. The low expression of autophagy genes, characteristic of CF cells, promoted us to examine transcriptional and translational regulation of autophagy molecules resulting from microRNA (miRNA, miR) and epigenetic variations. The study of microRNAs (miRNAs, miRs) continues to offer novel therapeutic targets. The objective of this study was to elucidate the role miRNAs play in the dysregulation of autophagy in CF macrophages and target them to restore this process and improve CFTR function. We identified the miR-17~92 cluster as a potential negative regulator of autophagy since CF macrophages exhibit increased cluster expression compared to wildtype (WT). The absence of the cluster increased autophagy protein expression, suggesting the canonical inverse relationship between miR-17~92 expression and autophagy gene expression which was further validated by luciferase assays. Downregulation of miR-17 and miR-20a restored autophagy expression in the lungs of CF mice. Notably, down-regulation of these inherently elevated miRNAs in vitro improved CFTR function, the fundamental cause of CF and its symptoms, via restoration of autophagy in macrophages.

Nutritional Epigenomics

Nutritional Epigenomics
Author : Anonim
Publisher : Academic Press
Release Date : 2019-07-20
Category : Medical
Total pages :478
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Nutritional Epigenomics offers a comprehensive overview of nutritional epigenomics as a mode of study, along with nutrition’s role in the epigenomic regulation of disease, health and developmental processes. Here, an expert team of international contributors introduces readers to nutritional epigenomic regulators of gene expression, our diet’s role in epigenomic regulation of disease and disease inheritance, caloric restriction and exercise as they relate to recent epigenomic findings, and the influence of nutritional epigenomics over circadian rhythms, aging and longevity, and fetal health and development, among other processes. Disease specific chapters address metabolic disease (obesity and diabetes), cancer, and neurodegeneration, among other disorders. Diet-gut microbiome interactions in the epigenomic regulation of disease are also discussed, as is the role of micronutrients and milk miRNAs in epigenetic regulation. Finally, chapter authors examine ongoing discussions of race and ethnicity in the social-epigenomic regulation of health and disease. Empowers the reader to employ nutritional epigenomics approaches in their own research Discusses the latest topics in nutritional epigenomics in the regulation of aging, circadian rhythm, inheritance and fetal development, as well as metabolism and disease Offers a full grounding in epigenetic reprogramming and nutritional intervention in the treatment and prevention of disease, as informed by population-based studies

Epigenetic Regulation of Stroke Recovery

Epigenetic Regulation of Stroke Recovery
Author : Michael D. Lowings
Publisher : Unknown
Release Date : 2011
Category :
Total pages :129
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Cross-talk Between Epigenetic Regulation and Mir-17~92 Cluster Expression in Idiopathic Pulmonary Fibrosis (IPF)

Cross-talk Between Epigenetic Regulation and Mir-17~92 Cluster Expression in Idiopathic Pulmonary Fibrosis (IPF)
Author : Duaa Dakhlallah
Publisher : Unknown
Release Date : 2011
Category :
Total pages :129
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Abstract: Interstitial lung disease/idiopathic pulmonary fibrosis (ILD/IPF) is the most progressive form of pulmonary fibrosis disorder and leads to death in patients afflicted. The etiology and pathogenesis of ILD/IPF in poorly understood with no known prevention or cure available. ILD/IPF is associated with increased expression of certain fibrogenic genes such as CTGF, VEGF, GM-CSF, and TSP-1; however, the precise mechanism responsible for the increased gene and protein expression is not known. Since there are a large number of genes differentially expressed in the lungs of patients with ILD/IPF compared to controls, we speculated that elements like microRNAs (miRNAs) may be involved. miRNAs, also known as miRs, are small regulatory RNAs that alter gene expression by causing degradation, translational repression, or epigenetic regulation resulting in a change in protein expression. Changes in miRNA expression are associated with up to 30% of cancers (Volinia et. al., 2010) and a variety of other diseases (Nana-Sinkam et. al., 2009). Using miRNA profiling, we identified a specific miRNA cluster that was reduced in expression in ILD/IPF lung tissue compared to normal lung tissue and lung tissue from patients with chronic obstructive pulmonary disease (COPD), the miR-17~92 cluster. The miR-17~92 polycistron cluster is ~ 1Kb located within the third intron of the open reading frame13q31.3 (C13orf25) which encodes six microRNAs (miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1 and miR-92a-1). This locus is overexpressed in B-cell lymphomas and lung cancer. In ILD/IPF, miR-17~92 miRNA cluster targets genes, such as metalloproteinases, collagen, and transforming growth factor that are highly expressed. Our preliminary data indicated decreased expression of the miR-17~92 miRNA cluster family members in the lungs from patients with ILD/IPF. Notably, miR-19b and miR-20a decreased proportionally to disease severity (and pulmonary function) of ILD/IPF. In ILD/IPF lung tissue, miR-19b and miR-20a expression was reduced and its predicted targets, CTGF, VEGF, TGF-[beta], TSP-1 and Ets-1 were up-regulated. Importantly, we noticed that the 5'-region of the promoter is heavily occupied with CpG Islands (>90%) and sought to define if this area was affected by methylation in ILD/IPF, as the mechanism causing downregulation of the cluster expression in ILD/IPF. Our preliminary data suggested that this epigenetic silencing of miR-17~92 clusters was due to methylation of the promoter, and was increased with the severity of ILD/IPF. Indeed, we found this CpG island methylated in ILD/IPF and by relieving this methylation with 5'-aza-2'-deoxycytidine, enhanced cluster expression and decreased expression of the target genes. In addition, we found that the miR-17~92 cluster targeted DNA methyltransferases (DNMTs), which we believe are responsible for the methylation events in ILD/IPF. Interestingly, our data showed direct regulation of miR-17, miR-19b, miR-20a and miR-92 on the 3'UTR of DNMT-1 in lung fibroblasts isolated from patients with IPF, indicating a negative feedback mechanism of the cluster to its own promoter though an epigenetic modifier. In fact, inhibition of DNA methylation by 5'-aza-2'-deoxycytidine in our in vivo murine bleomycin-induced pulmonary fibrosis model recovered miR-17~92 cluster expression to that of normal lung tissue, rescued the animals' lungs from fibrosis, and decreased fibrotic gene expression in their lungs. Thus, our data indicate that dysregulation of miRNA expression in IPF may contribute to the development and/or progression of the disease. 5'-aza-2'-deoxycytidine treatment, or miR-17~92 overexpression, could be a therapeutic intervention in ILD/IPF.