scholarly journals Heterochromatin: an epigenetic point of view in aging

2020 ◽  
Vol 52 (9) ◽  
pp. 1466-1474 ◽  
Author(s):  
Jong-Hyuk Lee ◽  
Edward W. Kim ◽  
Deborah L. Croteau ◽  
Vilhelm A. Bohr
Keyword(s):  
Aging Process ◽  
Epigenetic Modifications ◽  
Point Of View ◽  
Premature Aging ◽  
Epigenetic Changes ◽  
Chronological Aging ◽  
Functional Loss ◽  
Risk Of Mortality ◽  
Epigenetic Modulation ◽  
Reversible Nature

Abstract Aging is an inevitable process of life. Defined by progressive physiological and functional loss of tissues and organs, aging increases the risk of mortality for the organism. The aging process is affected by various factors, including genetic and epigenetic ones. Here, we review the chromatin-specific epigenetic changes that occur during normal (chronological) aging and in premature aging diseases. Taking advantage of the reversible nature of epigenetic modifications, we will also discuss possible lifespan expansion strategies through epigenetic modulation, which was considered irreversible until recently.

scholarly journals Metabolic Dysfunction in Hutchinson–Gilford Progeria Syndrome

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 395
Author(s):  
Ray Kreienkamp ◽  
Susana Gonzalo
Keyword(s):  
Aging Process ◽  
Therapeutic Potential ◽  
Normal Aging ◽  
Premature Aging ◽  
Metabolic Dysfunction ◽  
Epigenetic Changes ◽  
Patient Death ◽  
New Research ◽  
Progeria Syndrome ◽  
Hutchinson Gilford Progeria Syndrome

Hutchinson–Gilford Progeria Syndrome (HGPS) is a segmental premature aging disease causing patient death by early teenage years from cardiovascular dysfunction. Although HGPS does not totally recapitulate normal aging, it does harbor many similarities to the normal aging process, with patients also developing cardiovascular disease, alopecia, bone and joint abnormalities, and adipose changes. It is unsurprising, then, that as physicians and scientists have searched for treatments for HGPS, they have targeted many pathways known to be involved in normal aging, including inflammation, DNA damage, epigenetic changes, and stem cell exhaustion. Although less studied at a mechanistic level, severe metabolic problems are observed in HGPS patients. Interestingly, new research in animal models of HGPS has demonstrated impressive lifespan improvements secondary to metabolic interventions. As such, further understanding metabolism, its contribution to HGPS, and its therapeutic potential has far-reaching ramifications for this disease still lacking a robust treatment strategy.

Epigenetic Studies in Psychotherapy: A Systematic Review

2020 ◽  
Vol 16 (2) ◽  
pp. 86-92
Author(s):  
Rafael Penadés ◽  
Bárbara Arias ◽  
Mar Fatjó-Vilas ◽  
Laura González-Vallespí ◽  
Clemente García-Rizo ◽  
...  
Keyword(s):  
Systematic Review ◽  
Dna Methylation ◽  
Mental Disorders ◽  
Epigenetic Modifications ◽  
Symptom Improvement ◽  
Epigenetic Changes ◽  
Main Hypothesis ◽  
Psychological Treatments ◽  
Time Period ◽  
The Impact

Background: Epigenetic modifications appear to be dynamic and they might be affected by environmental factors. The possibility of influencing these processes through psychotherapy has been suggested. Objective: To analyse the impact of psychotherapy on epigenetics when applied to mental disorders. The main hypothesis is that psychological treatments will produce epigenetic modifications related to the improvement of treated symptoms. Methods: A computerised and systematic search was completed throughout the time period from 1990 to 2019 on the PubMed, ScienceDirect and Scopus databases. Results: In total, 11 studies were selected. The studies were evaluated for the theoretical framework, genes involved, type of psychotherapy and clinical challenges and perspectives. All studies showed detectable changes at the epigenetic level, like DNA methylation changes, associated with symptom improvement after psychotherapy. Conclusion: Methylation profiles could be moderating treatment effects of psychotherapy. Beyond the detected epigenetic changes after psychotherapy, the epigenetic status before the implementation could act as an effective predictor of response.

scholarly journals Epigenetic Modulation of TLR4 Expression by Sulforaphane Increases Anti-Inflammatory Capacity in Porcine Monocyte-Derived Dendritic Cells

Biology ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 490
Author(s):  
Xueqi Qu ◽  
Christiane Neuhoff ◽  
Mehmet Ulas Cinar ◽  
Maren Pröll ◽  
Ernst Tholen ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Dendritic Cells ◽  
Epigenetic Modifications ◽  
Dna Demethylation ◽  
Dependent Manner ◽  
Experimental Conditions ◽  
Hdac Activity ◽  
Protein Levels ◽  
Anti Inflammatory ◽  
Epigenetic Modulation

Inflammation is regulated by epigenetic modifications, including DNA methylation and histone acetylation. Sulforaphane (SFN), a histone deacetylase (HDAC) inhibitor, is also a potent immunomodulatory agent, but its anti-inflammatory functions through epigenetic modifications remain unclear. Therefore, this study aimed to investigate the epigenetic effects of SFN in maintaining the immunomodulatory homeostasis of innate immunity during acute inflammation. For this purpose, SFN-induced epigenetic changes and expression levels of immune-related genes in response to lipopolysaccharide (LPS) stimulation of monocyte-derived dendritic cells (moDCs) were analyzed. These results demonstrated that SFN inhibited HDAC activity and caused histone H3 and H4 acetylation. SFN treatment also induced DNA demethylation in the promoter region of the MHC-SLA1 gene, resulting in the upregulation of Toll-like receptor 4 (TLR4), MHC-SLA1, and inflammatory cytokines’ expression at 6 h of LPS stimulation. Moreover, the protein levels of cytokines in the cell culture supernatants were significantly inhibited by SFN pre-treatment followed by LPS stimulation in a time-dependent manner, suggesting that inhibition of HDAC activity and DNA methylation by SFN may restrict the excessive inflammatory cytokine availability in the extracellular environment. We postulate that SFN may exert a protective and anti-inflammatory function by epigenetically influencing signaling pathways in experimental conditions employing porcine moDCs.

scholarly journals Can Be miR-126-3p a Biomarker of Premature Aging? An Ex Vivo and In Vitro Study in Fabry Disease

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 356 ◽  
Author(s):  
Alessia Lo Curto ◽  
Simona Taverna ◽  
Maria Assunta Costa ◽  
Rosa Passantino ◽  
Giuseppa Augello ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Fabry Disease ◽  
Healthy Subjects ◽  
Aging Process ◽  
Replicative Senescence ◽  
Ex Vivo ◽  
Umbilical Vein ◽  
Quantitative Polymerase Chain Reaction ◽  
Premature Aging

Fabry disease (FD) is a lysosomal storage disorder (LSD) characterized by lysosomal accumulation of glycosphingolipids in a wide variety of cytotypes, including endothelial cells (ECs). FD patients experience a significantly reduced life expectancy compared to the general population; therefore, the association with a premature aging process would be plausible. To assess this hypothesis, miR-126-3p, a senescence-associated microRNA (SA-miRNAs), was considered as an aging biomarker. The levels of miR-126-3p contained in small extracellular vesicles (sEVs), with about 130 nm of diameter, were measured in FD patients and healthy subjects divided into age classes, in vitro, in human umbilical vein endothelial cells (HUVECs) “young” and undergoing replicative senescence, through a quantitative polymerase chain reaction (qPCR) approach. We confirmed that, in vivo, circulating miR-126 levels physiologically increase with age. In vitro, miR-126 augments in HUVECs underwent replicative senescence. We observed that FD patients are characterized by higher miR-126-3p levels in sEVs, compared to age-matched healthy subjects. We also explored, in vitro, the effect on ECs of glycosphingolipids that are typically accumulated in FD patients. We observed that FD storage substances induced in HUVECs premature senescence and increased of miR-126-3p levels. This study reinforces the hypothesis that FD may aggravate the normal aging process.

scholarly journals The work market awake for aged people

2007 ◽  
Vol 2 (1) ◽  
pp. 43-50
Author(s):  
Ana Maya Goto Uyehara
Keyword(s):  
Old Age ◽  
Aging Process ◽  
Point Of View ◽  
Professional Life ◽  
The Other ◽  
Job Market ◽  
Aged People ◽  
Current Concerns ◽  
Life Projects

At the end of XX century, the old age theme has been approached due to concern of the society with the quality of man’s life in the aging process and the fact of seniors correspond to a growing representative portion of the population in the quantitative point of view. So the aging changes in a problem that wins expressiveness and legitimacy in the field of the daily current concerns. This article intends to demonstrate that the work can articulate other life projects for the seniors and to avoid psychic pathologies in the old age that can appear due to the loss of personal identity, to the involvement lack in motivated activities or starting from the adoption of inadequate consumption ways or lifestyles. For this, this article assumes a line of preventive character explanation under two slopes: the first refers to the fact that, if the work ennobles the man, he must acquire or improve this individual competences, adapting them to the new demands of the job market to get a job, or even to reactivate his professional life because new life projects. The second slope follows the direction of the discovery of the seniors’ potentialities for the companies, which can adapt the qualities [and limitations] of this workers category to the various functions in the organization. The Brazilian entrepreneur needs to be attentive to the image of his company and the differential competitive that can distinguish it of the other companies. And this can be to employee senior people or to maintenance it in the company personnel staff.

A Review of epigenetics in psychiatry: focus on environmental risk factors

2020 ◽  
Vol 32 (1) ◽  
pp. 57-64
Author(s):  
Jessica Keverne ◽  
Elisabeth B. Binder
Keyword(s):  
Risk Factors ◽  
Psychiatric Disorders ◽  
Environmental Risk ◽  
Cell Function ◽  
Epigenetic Modifications ◽  
Environmental Risk Factors ◽  
Epigenetic Changes ◽  
Cell Type Specificity ◽  
Environmental Signals ◽  
Genetic And Environmental Factors

Abstract Epigenetic modifications play a key role in development and cell type specificity. These modifications seem to be particularly critical for brain development, where mutations in epigenetic enzymes have been associated with neurodevelopmental disorders as well as with the function of post-mitotic neurons. Epigenetic modifications can be influenced by genetic and environmental factors, both known major risk factors for psychiatric disorders. Epigenetic modifications may thus be an important mediator of the effects of genetic and environmental risk factors on cell function. This review summarizes the different types of epigenetic regulation and then focuses on the mechanisms transducing environmental signals, especially adverse life events that are major risk factors for psychiatric disorders, into lasting epigenetic changes. This is followed by examples of how the environment can induce epigenetic changes that relate to the risk of psychiatric disorders.

Aging, cellular senescence and cancer: epigenetic alterations and nuclear remodeling

2019 ◽  
pp. 238-253
Author(s):  
John C. Lucchesi
Keyword(s):  
Histone Modifications ◽  
Cellular Senescence ◽  
Aging Process ◽  
Nuclear Architecture ◽  
Gene Mutations ◽  
Histone Variants ◽  
Premature Aging ◽  
Model Organisms ◽  
Premature Aging Syndromes ◽  
Nuclear Remodeling

Epigenetic modifications correlated with aging and oncogenesis are changes in the pattern of DNA methylation and of histone modifications, and changes in the level of histone variants (H3.3, macroH2A, H2A.Z) and gene mutations. The sirtuins are a set of highly conserved protein deacetylases of particular significance to the aging process. Many cancer types are found to carry mutations in chromatin-modifying genes such as those encoding methyl or acetyl transferases, affecting the histone modifications of promoters and enhancers. The aging process and oncogenesis present a number of changes in the nuclear architecture. Mutations in the lamina-coding genes lead to premature aging syndromes. Mutations in remodeling complexes are found in different cancers. Modifications that affect the architectural protein binding sites at topologically associating domain (TAD) borders can cause the merging of neighboring TADs. The levels of short non-coding RNAs (sncRNAs) are altered in model organisms and are associated with cancer. Changes in the position of chromosome territories often occur in tumor cells. Nevertheless, cellular senescence, due mostly to the absence of telomerase, represents a mechanism of tumor suppression.

scholarly journals Epigenetics of Meningiomas

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Balázs Murnyák ◽  
László Bognár ◽  
Álmos Klekner ◽  
Tibor Hortobágyi
Keyword(s):  
Dna Methylation ◽  
Central Nervous System ◽  
Genetic Alterations ◽  
Chromatin Modifications ◽  
Epigenetic Changes ◽  
Epigenetic Alterations ◽  
Central Nervous System Tumours ◽  
Growing Body ◽  
Tumour Initiation ◽  
Reversible Nature

Meningiomas account for one-third of all adult central nervous system tumours and are divided into three WHO grades. In contrast to the relatively well characterized genetic alterations, our current understanding of epigenetic modifications involved in the meningioma-genesis and progression is rather incomplete. Contrary to genetic alterations, epigenetic changes do not alter the primary DNA sequence and their reversible nature serves as an excellent basis for prevention and development of novel personalised tumour therapies. Indeed, growing body of evidence suggests that disturbed epigenetic regulation plays a key role in the pathogenesis of meningiomas. Altered DNA methylation, microRNA expression, histone, and chromatin modifications are frequently noted in meningiomas bearing prognostic and therapeutic relevance. In this review we provide an overview on recently identified epigenetic alterations in meningiomas and discuss their role in tumour initiation, progression, and recurrence.

scholarly journals New Insights into Chronological Mobility of Retrotransposons In Vivo

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Amr. R. Ghanam ◽  
Jun Cao ◽  
Xuan Ouyang ◽  
Xiaoyuan Song
Keyword(s):  
Aging Process ◽  
Therapeutic Interventions ◽  
Chronological Aging ◽  
Mouse Tissues ◽  
Biological Compounds ◽  
Physiological Homeostasis ◽  
Tissue Aging ◽  
Cell Expression ◽  
Different Tissues

Tissue aging is the gradual decline of physiological homeostasis accompanied with accumulation of senescent cells, decreased clearance of unwanted biological compounds, and depletion of stem cells. Senescent cells were cell cycle arrested in response to various stimuli and identified using distinct phenotypes and changes in gene expression. Senescent cells that accumulate with aging can compromise normal tissue function and inhibit or stop repair and regeneration. Selective removal of senescent cells can slow the aging process and inhibits age-associated diseases leading to extended lifespans in mice and thus provides a possibility for developing antiaging therapy. To monitor the appearance of senescent cells in vivo and target them, a clearer understanding of senescent cell expression markers is needed. We investigated the age-associated expression of three molecular hallmarks of aging: SA-β-gal, P16INK4a, and retrotransposable elements (RTEs), in different mouse tissues during chronological aging. Our data showed that the expression of these markers is variable with aging in the different tissues. P16INK4a showed consistent increases with age in most tissues, while expression of RTEs was variable among different tissues examined. These data suggest that biological changes occurring with physiological aging may be useful in choosing the appropriate timing of therapeutic interventions to slow the aging process or keep more susceptible organs healthier in the aging process.

scholarly journals EPIGENETIC PROFILES OF BIOLOGICAL AGING HALLMARKS

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S424-S424
Author(s):  
Diana L Leung ◽  
Zuyun Liu ◽  
Morgan E Levine
Keyword(s):  
Aging Process ◽  
Strong Association ◽  
Cpg Islands ◽  
Biological Aging ◽  
Epigenetic Alterations ◽  
Chronological Aging ◽  
Progeroid Syndromes ◽  
Progeria Syndrome ◽  
Hutchinson Gilford Progeria Syndrome ◽  
Weighted Network Analysis

Abstract Investigation into the hallmarks of aging point to the existence of shared mechanisms that underlie the biological aging process. While there is a general consensus that hallmarks of aging rarely occur in isolation, little is known in regards to their overlapping networks or how interactions contribute to manifestations at the clinical level. Here, we examine whether shared epigenetic alterations—one of the proposed hallmark of aging—underlies diverse conditions characterized by other hallmarks, including cellular senescence, loss of proteostasis, genomic instability, mitochondrial dysfunction, and inflammation. Using weighted network analysis, we identified consistent overlaps in the methylation profiles across the different traits. For instance, epigenetic modules that were distinct in senescence were also affected in progeroid syndromes (Hutchinson-Gilford Progeria Syndrome and Werner’s Syndrome) and smokers. These CpGs tended to be located in CpG islands, which are notable for their strong association with transcriptional regulation. Overall, our results suggest that epigenetic alterations intersect with various hallmarks of aging. In moving forward, incorporation of this understanding may lead to the development of biomarkers that better capture the biological (rather than chronological) aging process.

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