scholarly journals Epigenetic Regulation of Skin Cells in Natural Aging and Premature Aging Diseases

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 268 ◽  
Author(s):  
Donata Orioli ◽  
Elena Dellambra
Keyword(s):  
Accelerated Aging ◽  
Natural Aging ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Premature Aging ◽  
Telomere Shortening ◽  
Skin Cells ◽  
Skin Cell ◽  
Progeroid Syndromes

Skin undergoes continuous renewal throughout an individual’s lifetime relying on stem cell functionality. However, a decline of the skin regenerative potential occurs with age. The accumulation of senescent cells over time probably reduces tissue regeneration and contributes to skin aging. Keratinocytes and dermal fibroblasts undergo senescence in response to several intrinsic or extrinsic stresses, including telomere shortening, overproduction of reactive oxygen species, diet, and sunlight exposure. Epigenetic mechanisms directly regulate skin homeostasis and regeneration, but they also mark cell senescence and the natural and pathological aging processes. Progeroid syndromes represent a group of clinical and genetically heterogeneous pathologies characterized by the accelerated aging of various tissues and organs, including skin. Skin cells from progeroid patients display molecular hallmarks that mimic those associated with naturally occurring aging. Thus, investigations on progeroid syndromes strongly contribute to disclose the causal mechanisms that underlie the aging process. In the present review, we discuss the role of epigenetic pathways in skin cell regulation during physiologic and premature aging.

scholarly journals Altered Nuclear Functions in Progeroid Syndromes: a Paradigm for Aging Research

2009 ◽  
Vol 9 ◽  
pp. 1449-1462 ◽  
Author(s):  
Baomin Li ◽  
Sonali Jog ◽  
Jose Candelario ◽  
Sita Reddy ◽  
Lucio Comai
Keyword(s):  
Werner Syndrome ◽  
Accelerated Aging ◽  
Natural Aging ◽  
Aging Research ◽  
Cellular Processes ◽  
Functional Connections ◽  
Age Related ◽  
Progeroid Syndromes ◽  
Progeria Syndrome ◽  
Hutchinson Gilford Progeria Syndrome

Syndromes of accelerated aging could provide an entry point for identifying and dissecting the cellular pathways that are involved in the development of age-related pathologies in the general population. However, their usefulness for aging research has been controversial, as it has been argued that these diseases do not faithfully reflect the process of natural aging. Here we review recent findings on the molecular basis of two progeroid diseases, Werner syndrome (WS) and Hutchinson-Gilford progeria syndrome (HGPS), and highlight functional connections to cellular processes that may contribute to normal aging.

Adolescent Obesity and Eating Disorders: Can Calorie Restriction have a Positive Impact

2020 ◽  
Vol 16 (4) ◽  
pp. 433-443
Author(s):  
Naveen Visweswaraiah ◽  
Kousalya Nathan
Keyword(s):  
Calorie Restriction ◽  
Lifestyle Modification ◽  
Positive Impact ◽  
Food Preferences ◽  
Accelerated Aging ◽  
Adolescent Obesity ◽  
Premature Aging ◽  
Pharmacological Intervention ◽  
The Impact

Background: The current obesogenic environment with relatively increased affordability and availability of high calorie food and beverages, has led to an alarming increase in the prevalence of obesity and related lifestyle disorders in children and adolescents, predisposing them to accelerated aging. The increased prevalence may be due to the eating behavior of adolescents, their genetic and molecular etiology and/or due to the impact of psychological stress and their wrong lifestyle choices. Calorie restriction has been extensively researched for reducing the obesity in adolescents and adults but is yet to be successfully implemented. Objective: The present review paper focuses on the types of calorie restriction diets, the role of its mimics and the nutrigenomic mechanisms that may be helpful in reducing obesity and related disorders in the adolescents. The role of behavioral therapeutic techniques and physical activity has also been highlighted in addition to the calorie restricted diet for bringing about an overall lifestyle modification in the management of obesity. Conclusion: Food preferences are acquired in childhood and sound nutritional practices should be established in childhood to prevent lifestyle disorders and premature aging. Though CR is a known and preferred non-pharmacological intervention in the management of obesity, its implemention has not been explored and evaluated extensively. This is a vital area that needs scientific research as the goals of obesity managements are no longer just weight loss through dietary restrictions. An interdisciplinary method to lifestyle modification in the management of adolescent obesity addressing all physiological and psychosocial aspects is recommended.

scholarly journals Exopolysaccharide from Lactobacillus plantarum HY7714 Protects against Skin Aging through Skin–Gut Axis Communication

Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1651
Author(s):  
Kippeum Lee ◽  
Hyeon Ji Kim ◽  
Soo A Kim ◽  
Soo-Dong Park ◽  
Jae-Jung Shim ◽  
...  
Keyword(s):  
Tight Junctions ◽  
Lactobacillus Plantarum ◽  
Skin Diseases ◽  
Therapeutic Potential ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Skin Damage ◽  
Genes Encoding ◽  
Natural Result

Skin aging occurs inevitably as a natural result of physiological changes over time. In particular, solar exposure of the skin accounts for up to 90% of skin damage. Numerous studies have examined the ability of dietary constituents to prevent skin aging, and recent research has emphasized the role of functional probiotics in intestinal function and skin aging. However, the mechanism of the interactions between aging and probiotics has not been elucidated yet. The aim of this study was to determine the role of exopolysaccharides (EPS) produced by lactic acid bacteria (LAB) identified as Lactobacillus plantarum HY7714 in regulating tight junctions in intestinal epithelial cells and increasing moisture retention in human dermal fibroblasts cells. We observed that HY7714 EPS controlled intestinal tight junctions in Caco-2 cells by upregulating the genes encoding occludin-1 (OCL-1) and zonula occluden-1 (ZO-1). In addition, HY7714 EPS effectively improved UVB-induced cytotoxicity and hydration capacity in HS68 cells by downregulating production of metalloproteinases (MMPs) and reactive oxygen species (ROS). In summary, HY7714 EPS is an effective anti-aging molecule in skin and may have therapeutic potential against skin diseases and UVB-induced damage. Therefore, HY7714 EPS serves as a functional substance in skin–gut axis communication.

scholarly journals Rapamycin Protects Skin Fibroblasts From UVA-Induced Photoaging by Inhibition of p53 and Phosphorylated HSP27

2021 ◽  
Vol 9 ◽  
Author(s):  
Gen-Long Bai ◽  
Ping Wang ◽  
Xin Huang ◽  
Zi-Yue Wang ◽  
Di Cao ◽  
...  
Keyword(s):  
Type I Collagen ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Aging Effects ◽  
Smad Signaling Pathway ◽  
Skin Photoaging ◽  
Dermal Collagen ◽  
Induced Apoptosis

Skin aging caused by UV radiation is called photoaging is characterized by skin roughness and dryness accompanied by a significant reduction of dermal collagen. Rapamycin is a macrolide immunosuppressant which has been shown to exhibit “anti-aging” effects in cells and organisms, however, its roles in the skin photoaging remains unclear. Here, we investigate the role of rapamycin and HSP27, which we have previously identified as an inhibitor of UV-induced apoptosis and senescence in HaCat cells, in a UVA-induced photoaging model of primary human dermal fibroblasts (HDFs). Results from senescence-associated beta-galactosidase (SA-β-gal) staining revealed that rapamycin significantly reduced senescence in UVA-treated HDFs. In addition, treatment with rapamycin significantly increased cell autophagy levels, decreased the expression of p53 and phosphorylated HSP27, and reduced genotoxic and oxidative cellular stress levels in UVA-induced HDFs. Knockdown of HSP27 resulted in a significant increase of MMP-1 and MMP-3 as well as a decrease in type I collagen expression. Rapamycin mitigated these effects by activation of the classical TGF-β/Smad signaling pathway and increasing the transcriptional activity of MAPK/AP-1. Taken together, these results suggest that rapamycin may potentially serve as a preventive and therapeutic agent for UVA-induced photoaging of the skin.

scholarly journals Role of Glycosidic Aroma Precursors on the odorant profiles of Grenache noir and Syrah Wines from the Rhone valley. Part 2: characterisation of derived compounds

OENO One ◽  
2009 ◽  
Vol 43 (4) ◽  
pp. 213
Author(s):  
Marie A. Segurel ◽  
Raymond L. Baumes ◽  
Dominique Langlois ◽  
Christine Riou ◽  
Alain Razungles
Keyword(s):  
Multivariate Analyses ◽  
Accelerated Aging ◽  
Natural Aging ◽  
Aroma Compounds ◽  
Varietal Differences ◽  
Aroma Precursors ◽  
Rhone Valley ◽  
Grape Varieties ◽  
Related Compounds

<p style="text-align: justify;"><strong>Aims</strong>: Grenache noir and Syrah are the predominant grape varieties in the French Rhone valley vineyard. This study aimed at identifying the odorants generated from glycoconjugates extracted from wines made with Grenache noir and Syrah.</p><p style="text-align: justify;"><strong>Methods and results</strong>: Synthetic model wines enriched with glycoconjugates, treated or not with enzymes, were stored at 45 °C for 3 weeks, or at 13 °C for 18 months. Aromas generated were extracted and analyzed by GC-Olfactometry (only samples from accelerated aging) and were further quantitatively determined by GC-MS. Analysis of the extracts allowed to identify 49 odorants, including 27 that could be aglycons, or related compounds, of glycoconjugates from the grapes. In addition, the active compounds were quantified in similar experiments led in conditions of natural aging for 18 months.</p><p style="text-align: justify;"><strong>Conclusion</strong>: The two varieties, Grenache noir and Syrah, were distinguishable by 14 odorant zones. Multivariate analyses (PCA) performed with the amounts of aroma compounds formed during both model and natural aging confirmed the effect of the glycosidase treatment on the acceleration of the aroma compounds formation and on the increase of the varietal differences of the wines.</p><p style="text-align: justify;"><strong>Significance and impact of study</strong>: GC-Olfactometry coupled with GCMS were good techniques to indentify and apreciate the odorants generated from glycoconjugates in the wines of Syrah and Grenache Noir, but in the context of a blend of odors, these techniques showed their limits and did not permit to determine the real impact of a molecule in the global aroma of the wine perceived by the taster. Other methods as additive techniques should be used to complete this study.</p>

scholarly journals Age Associated Decrease of MT-1 Melatonin Receptor in Human Dermal Skin Fibroblasts Impairs Protection Against UV-Induced DNA Damage

2020 ◽  
Vol 21 (1) ◽  
pp. 326
Author(s):  
Kelly Dong ◽  
Earl Goyarts ◽  
Antonella Rella ◽  
Edward Pelle ◽  
Yung Hou Wong ◽  
...  
Keyword(s):  
Dna Damage ◽  
Circadian Rhythm ◽  
Human Skin ◽  
Human Body ◽  
Skin Aging ◽  
Skin Fibroblasts ◽  
Melatonin Receptor ◽  
Skin Cells ◽  
Normal Human

The human body follows a physiological rhythm in response to the day/night cycle which is synchronized with the circadian rhythm through internal clocks. Most cells in the human body, including skin cells, express autonomous clocks and the genes responsible for running those clocks. Melatonin, a ubiquitous small molecular weight hormone, is critical in regulating the sleep cycle and other functions in the body. Melatonin is present in the skin and, in this study, we showed that it has the ability to dose-dependently stimulate PER1 clock gene expression in normal human dermal fibroblasts and normal human epidermal keratinocytes. Then we further evaluated the role of MT-1 melatonin receptor in mediating melatonin actions on human skin using fibroblasts derived from young and old subjects. Using immunocytochemistry, Western blotting and RT-PCR, we confirmed the expression of MT-1 receptor in human skin fibroblasts and demonstrated a dramatic age-dependent decrease in its level in mature fibroblasts. We used siRNA technology to transiently knockdown MT-1 receptor in fibroblasts. In these MT-1 knockdown cells, UV-dependent oxidative stress (H2O2 production) was enhanced and DNA damage was also increased, suggesting a critical role of MT-1 receptor in protecting skin cells from UV-induced DNA damage. These studies demonstrate that the melatonin pathway plays a pivotal role in skin aging and damage. Moreover, its correlation with skin circadian rhythm may offer new approaches for decelerating skin aging by modulating the expression of melatonin receptors in human skin.

The Possible Role of Telomere Length and Chemokines in the Aging Process: A Transdiagnostic Review in Psychiatry

2019 ◽  
Vol 15 (3) ◽  
pp. 171-192
Author(s):  
Fernanda Endler Valiati ◽  
Gabriel Henrique Hizo ◽  
Jairo Vinícius Pinto ◽  
Márcia Kauer-Sant`Anna
Keyword(s):  
Psychiatric Disorders ◽  
Telomere Length ◽  
Aging Process ◽  
Accelerated Aging ◽  
Premature Death ◽  
Mental Illnesses ◽  
Telomere Shortening ◽  
Early Aging ◽  
The Relationship

Background: Psychiatric disorders are common, reaching a worldwide prevalence of 29.2%. They are associated with a high risk of premature death and with accelerated aging in clinical, molecular and neuroimaging studies. Recently, there is strong evidence suggesting a possible role of telomere length and chemokines in aging processes in psychiatric disorders. Objective: We aimed to review the literature on telomere length and chemokines and its association with early aging in mental illnesses on a transdiagnostic approach. Results: The review highlights the association between psychiatric disorders and early aging. Several independent studies have reported shorter telomere length and dysregulations on levels of circulating chemokines in schizophrenia, bipolar disorder, major depressive disorder, and anxiety disorders, suggesting a complex interaction between these markers in a transdiagnostic level. However, studies have investigated the inflammatory markers and telomere shortening separately and associated with a particular diagnosis, rather than as a transdiagnostic biological feature. Conclusion: There is consistent evidence supporting the relationship between accelerated aging, telomere length, and chemokines in mental disorders, but they have been studied individually. Thus, more research is needed to improve the knowledge of accelerated senescence and its biomarkers in psychiatry, not only individually in each diagnosis, but also based on a transdiagnostic perspective. Moreover, further research should try to elucidate how the intricate association between the chemokines and telomeres together may contribute to the aging process in psychiatric disorders.

scholarly journals Hereditary syndromes with signs of premature aging

2020 ◽  
Vol 22 (3) ◽  
pp. 4-18
Author(s):  
Olga O. Golounina ◽  
Valentin V. Fadeev ◽  
Zhanna E. Belaya
Keyword(s):  
Molecular Mechanisms ◽  
Werner Syndrome ◽  
Accelerated Aging ◽  
Scientific Data ◽  
The Body ◽  
Premature Aging ◽  
Hereditary Diseases ◽  
Age Related ◽  
Progeroid Syndromes ◽  
Age Related Changes

Aging is a multi-factor biological process that inevitably affects everyone. Degenerative processes, starting at the cellular and molecular levels, gradually influence the change in the functional capabilities of all organs and systems. Progeroid syndromes (from Greek. progērōs prematurely old), or premature aging syndromes, represent clinically and genetically heterogeneous group of rare hereditary diseases characterized by accelerated aging of the body. Progeria and segmental progeroid syndromes include more than a dozen diseases, but the most clear signs of premature aging are evident in Hutchinson-Guilford Progeria Syndrome and Werner Syndrome. This review summarizes the latest scientific data reflecting the etiology and clinical picture of progeria and segmental progeroid syndromes in humans. Molecular mechanisms of aging are considered, using the example of progeroid syndromes. Modern possibilities and potential ways of influencing the mechanisms of the development of age-related changes are discussed. Further study of genetic causes, as well as the development of treatment for progeria and segmental progeroid syndromes, may be a promising direction for correcting age-related changes and increasing life expectancy.

scholarly journals Outcomes of 4 years of molecular genetic diagnosis on a panel of genes involved in premature aging syndromes, including laminopathies and related disorders

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Maude Grelet ◽  
Véronique Blanck ◽  
Sabine Sigaudy ◽  
Nicole Philip ◽  
Fabienne Giuliano ◽  
...  
Keyword(s):  
Molecular Diagnosis ◽  
High Throughput ◽  
High Throughput Sequencing ◽  
Diagnostic Yield ◽  
Genetic Diagnosis ◽  
Natural Aging ◽  
Premature Aging ◽  
Pathogenic Variants ◽  
Progeroid Syndromes ◽  
Premature Aging Syndromes

Abstract Background Segmental progeroid syndromes are a heterogeneous group of rare and often severe genetic disorders that have been studied since the twentieth century. These progeroid syndromes are defined as segmental because only some of the features observed during natural aging are accelerated. Methods Since 2015, the Molecular Genetics Laboratory in Marseille La Timone Hospital proposes molecular diagnosis of premature aging syndromes including laminopathies and related disorders upon NGS sequencing of a panel of 82 genes involved in these syndromes. We analyzed the results obtained in 4 years on 66 patients issued from France and abroad. Results Globally, pathogenic or likely pathogenic variants (ACMG class 5 or 4) were identified in about 1/4 of the cases; among these, 9 pathogenic variants were novel. On the other hand, the diagnostic yield of our panel was over 60% when the patients were addressed upon a nosologically specific clinical suspicion, excepted for connective tissue disorders, for which clinical diagnosis may be more challenging. Prenatal testing was proposed to 3 families. We additionally detected 16 variants of uncertain significance and reclassified 3 of them as benign upon segregation analysis in first degree relatives. Conclusions High throughput sequencing using the Laminopathies/ Premature Aging disorders panel allowed molecular diagnosis of rare disorders associated with premature aging features and genetic counseling for families, representing an interesting first-level analysis before whole genome sequencing may be proposed, as a future second step, by the National high throughput sequencing platforms (“Medicine France Genomics 2025” Plan), in families without molecular diagnosis.

scholarly journals Junctional adhesion molecule-A is abnormally expressed in diffuse cutaneous systemic sclerosis skin and mediates myeloid cell adhesion

2009 ◽  
Vol 69 (01) ◽  
pp. 249-254 ◽  
Author(s):  
Y Hou ◽  
B J Rabquer ◽  
M L Gerber ◽  
F Del Galdo ◽  
S A Jimenez ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Systemic Sclerosis ◽  
Adhesion Molecule ◽  
Dermal Fibroblast ◽  
Myeloid Cell ◽  
Dermal Fibroblasts ◽  
Normal Volunteers ◽  
Skin Cell ◽  
Diffuse Cutaneous Systemic Sclerosis

Objective:To investigate the role of junctional adhesion molecule-A (JAM-A) in the pathogenesis of systemic sclerosis (SSc).Methods:Biopsy specimens from proximal and distal arm skin and serum were obtained from patients with SSc and normal volunteers. To determine the expression of JAM-A on SSc dermal fibroblasts and in SSc skin, cell surface ELISAs and immunohistology were performed. An ELISA was designed to determine the amount of soluble JAM-A (sJAM-A) in serum. Myeloid U937 cell–SSc dermal fibroblast and skin adhesion assays were performed to determine the role of JAM-A in myeloid cell adhesion.Results:The stratum granulosum and dermal endothelial cells (ECs) from distal arm SSc skin exhibited significantly decreased expression of JAM-A in comparison with normal volunteers. However, sJAM-A was increased in the serum of patients with SSc compared with normal volunteers. Conversely, JAM-A was increased on the surface of SSc compared with normal dermal fibroblasts. JAM-A accounted for a significant portion of U937 binding to SSc dermal fibroblasts. In addition, JAM-A contributed to U937 adhesion to both distal and proximal SSc skin.Conclusions:JAM-A expression is dysregulated in SSc skin. Decreased expression of JAM-A on SSc ECs may result in a reduced response to proangiogenic basic fibroblast growth factor. Increased JAM-A expression on SSc fibroblasts may serve to retain myeloid cells, which in turn secrete angiogenic factors.

Sign in / Sign up

Export Citation Format

Share Document