scholarly journals Epigenetic Mechanisms of Paternal Stress in Offspring Development and Diseases

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Xingyun Xu ◽  
Zhigang Miao ◽  
Miao Sun ◽  
Bo Wan

The major biological function of the sperm cell is to transmit the paternal genetic and epigenetic information to the embryo as well as the following offspring. Sperm has a unique epigenome. An increasing body of epidemiological study supports that paternal stress induced by environmental exposures and lifestyle can modulate the sperm epigenome (including histone modification, DNA methylation, and noncoding RNA expression), sperm-egg fusion, embryo development, and offspring health. Based on the existing literature, we have summarized the paternal exposure on sperm epigenome along with the representative phenotypes of offspring and the possible mechanism involved.

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 759
Author(s):  
Zhongjing Su ◽  
Guangyu Liu ◽  
Bin Zhang ◽  
Ze Lin ◽  
Dongyang Huang

The leukocyte common antigen CD45 is a transmembrane phosphatase expressed on all nucleated hemopoietic cells, and the expression levels of its splicing isoforms are closely related to the development and function of lymphocytes. PEBP1P3 is a natural antisense transcript from the opposite strand of CD45 intron 2 and is predicted to be a noncoding RNA. The genotype-tissue expression and quantitative PCR data suggested that PEBP1P3 might be involved in the regulation of expression of CD45 splicing isoforms. To explore the regulatory mechanism of PEBP1P3 in CD45 expression, DNA methylation and histone modification were detected by bisulfate sequencing PCR and chromatin immunoprecipitation assays, respectively. The results showed that after the antisense RNA PEBP1P3 was knocked down by RNA interference, the DNA methylation of CD45 intron 2 was decreased and histone H3K9 and H3K36 trimethylation at the alternative splicing exons of CD45 DNA was increased. Knockdown of PEBP1P3 also increased the binding levels of chromatin conformation organizer CTCF at intron 2 and the alternative splicing exons of CD45. The present results indicate that the natural antisense RNA PEBP1P3 regulated the alternative splicing of CD45 RNA, and that might be correlated with the regulation of histone modification and DNA methylation.


2015 ◽  
Vol 16 (12) ◽  
pp. 29732-29743 ◽  
Author(s):  
Agnieszka Kaufman-Szymczyk ◽  
Grzegorz Majewski ◽  
Katarzyna Lubecka-Pietruszewska ◽  
Krystyna Fabianowska-Majewska

Author(s):  
Fei Xu ◽  
Wenhui Li ◽  
Xiao Yang ◽  
Lixin Na ◽  
Linjun Chen ◽  
...  

Osteoporosis is a metabolic disease characterized by decreased bone mineral density and the destruction of bone microstructure, which can lead to increased bone fragility and risk of fracture. In recent years, with the deepening of the research on the pathological mechanism of osteoporosis, the research on epigenetics has made significant progress. Epigenetics refers to changes in gene expression levels that are not caused by changes in gene sequences, mainly including DNA methylation, histone modification, and non-coding RNAs (lncRNA, microRNA, and circRNA). Epigenetics play mainly a post-transcriptional regulatory role and have important functions in the biological signal regulatory network. Studies have shown that epigenetic mechanisms are closely related to osteogenic differentiation, osteogenesis, bone remodeling and other bone metabolism-related processes. Abnormal epigenetic regulation can lead to a series of bone metabolism-related diseases, such as osteoporosis. Considering the important role of epigenetic mechanisms in the regulation of bone metabolism, we mainly review the research progress on epigenetic mechanisms (DNA methylation, histone modification, and non-coding RNAs) in the osteogenic differentiation and the pathogenesis of osteoporosis to provide a new direction for the treatment of bone metabolism-related diseases.


STEMedicine ◽  
2020 ◽  
Vol 1 (1) ◽  
pp. e5
Author(s):  
Xiuzhi Jia ◽  
Hao Cheng ◽  
Ying Xiao

As a group of autoimmune diseases, systemic sclerosis (scleroderma, SSc) is characterized by immune dysregulation, micro-vessels dominant obliteration, and the final fibrosis of the skin and or internal organs. Although the precise mechanisms are still unknown, increasing data shows that epigenetic mechanisms, such as DNA methylation, histone modification, and microRNA (miRNA), are strictly related to the pathogenesis of scleroderma. Epigenetic mechanisms, which can link genetics and environmental stress, represents a promising field in systemic sclerosis investigation. The objective of this review is, to sum up the current information about epigenetic alteration.


Diabetologia ◽  
2019 ◽  
Vol 62 (12) ◽  
pp. 2171-2178 ◽  
Author(s):  
Hannah R. Elliott ◽  
Gemma C. Sharp ◽  
Caroline L. Relton ◽  
Deborah A. Lawlor

Abstract Epigenetics encapsulates a group of molecular mechanisms including DNA methylation, histone modification and microRNAs (miRNAs). Gestational diabetes (GDM) increases the risk of adverse perinatal outcomes and is associated with future offspring risk of obesity and type 2 diabetes. It has been hypothesised that epigenetic mechanisms mediate an effect of GDM on offspring adiposity and type 2 diabetes and this could provide a modifiable mechanism to reduce type 2 diabetes in the next generation. Evidence for this hypothesis is lacking. Epigenetic epidemiology could also contribute to reducing type 2 diabetes by identifying biomarkers that accurately predict risk of GDM and its associated future adverse outcomes. We reviewed published human studies that explored associations between any of maternal GDM, type 2 diabetes, gestational fasting or post-load glucose and any epigenetic marker (DNA methylation, histone modification or miRNA). Of the 81 relevant studies we identified, most focused on the potential role of epigenetic mechanisms in mediating intrauterine effects of GDM on offspring outcomes. Studies were small (median total number of participants 58; median number of GDM cases 27) and most did not attempt replication. The most common epigenetic measure analysed was DNA methylation. Most studies that aimed to explore epigenetic mediation examined associations of in utero exposure to GDM with offspring cord or infant blood/placenta DNA methylation. Exploration of any causal effect, or effect on downstream offspring outcomes, was lacking. There is a need for more robust methods to explore the role of epigenetic mechanisms as possible mediators of effects of exposure to GDM on future risk of obesity and type 2 diabetes. Research to identify epigenetic biomarkers to improve identification of women at risk of GDM and its associated adverse (maternal and offspring) outcomes is currently rare but could contribute to future tools for accurate risk stratification.


2021 ◽  
Vol 11 ◽  
Author(s):  
Xiangzhen Wei ◽  
Menghua Cai ◽  
Lifang Jin

Parkinson’s means Parkinson’s disease, a chronic degenerative disease of central nervous system. The main area which is affected by this disease is motor system. Since it firstly founded by James Parkinson in his 1817 publication, nowadays, people still have lots of questions about this disease. This review mainly summarizes the epigenetics of Parkinson’s. DNA methylation is one of the epigenetic mechanisms of Parkinson’s. During the development of disease, global hypomethylation, and hypermethylation happen in different areas of patients. Another epigenetic mechanism is histone modification. People believe that some metals can induce Parkinson’s disease by modulating epigenetic mechanisms. This review summarizes the relationships between different metals and Parkinson’s disease. However, the specific roles of most metals in epigenetics are still unknown, which need further research.


2020 ◽  
Vol 7 (1) ◽  
pp. 309-331
Author(s):  
Yonggang Pei ◽  
Josiah Hiu-yuen Wong ◽  
Erle S. Robertson

Among all of the known biological carcinogens, Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) are two of the classical oncogenic herpesviruses known to induce the oncogenic phenotype. Many studies have revealed important functions related to epigenetic alterations of the EBV and KSHV genomes that mediate oncogenesis, but the detailed mechanisms are not fully understood. It is also challenging to fully describe the critical cellular events that drive oncogenesis as well as a comprehensive map of the molecular contributors. This review introduces the roles of epigenetic modifications of these viral genomes, including DNA methylation, histone modification, chromatin remodeling, and noncoding RNA expression, and elucidates potential strategies utilized for inducing oncogenesis by these human gammaherpesviruses.


2018 ◽  
Vol 177 (3) ◽  
pp. 1187-1197 ◽  
Author(s):  
Feng Tan ◽  
Yue Lu ◽  
Wei Jiang ◽  
Tian Wu ◽  
Ruoyu Zhang ◽  
...  

2021 ◽  
Vol 22 (16) ◽  
pp. 8921
Author(s):  
Émile Bélanger ◽  
Catherine Laprise

Epigenetics is a field of study investigating changes in gene expression that do not alter the DNA sequence. These changes are often influenced by environmental or social factors and are reversible. Epigenetic mechanisms include DNA methylation, histone modification, and noncoding RNA. Understanding the role of these epigenetic mechanisms in human diseases provides useful information with regard to disease severity and development. Several studies have searched for the epigenetic mechanisms that regulate allergies and asthma; however, only few studies have used samples of eosinophil, a proinflammatory cell type known to be largely recruited during allergic or asthmatic inflammation. Such studies would enable us to better understand the factors that influence the massive recruitment of eosinophils during allergic and asthmatic symptoms. In this review, we sought to summarize different studies that aimed to discover differential patterns of histone modifications, DNA methylation, and noncoding RNAs in eosinophil samples of individuals with certain diseases, with a particular focus on those with asthma or allergic diseases.


2018 ◽  
Author(s):  
Elmar W Tobi ◽  
Joost van den Heuvel ◽  
Bas J. Zwaan ◽  
L.H. Lumey ◽  
Bastiaan T. Heijmans ◽  
...  

AbstractMaternal adversity is associated with long-term physiological changes in offspring. These are believed to be mediated through epigenetic mechanisms, including DNA methylation (DNAm). Changes in DNAm are often interpreted as damage or as part of plastic responses of the embryo. We propose that selection on stochastic DNAm differences generated during epigenetic reprogramming after fertilization contributes to the effects of maternal adversity on DNAm. Using a mathematical model of epigenetic reprogramming in the early embryo we predict that this “epigenetic selection” will generate a characteristic reduction in variance of DNAm at selected loci in populations exposed to maternal adversity. We tested this prediction using DNAm data from a human cohort prenatally exposed to the Dutch Famine and confirmed the reduction in DNAm variance, suggesting that epigenetic selection may have occurred. Epigenetic selection should be considered as a possible mechanism linking adversity in pregnancy to offspring health and may have implications for the likely effectiveness of intervention strategies.


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