scholarly journals A-type lamins and cardiovascular disease in premature aging syndromes

2017 ◽  
Vol 46 ◽  
pp. 17-25 ◽  
Author(s):  
Beatriz Dorado ◽  
Vicente Andrés
Keyword(s):  
Cardiovascular Disease ◽  
Premature Aging ◽  
Premature Aging Syndromes

Understanding Vascular Diseases: Lessons From Premature Aging Syndromes

2016 ◽  
Vol 32 (5) ◽  
pp. 650-658 ◽  
Author(s):  
Yuichi Ikeda ◽  
Hidetoshi Kumagai ◽  
Yoshihiro Motozawa ◽  
Jun-ichi Suzuki ◽  
Hiroshi Akazawa ◽  
...  
Keyword(s):  
Vascular Diseases ◽  
Premature Aging ◽  
Premature Aging Syndromes

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.

O VI.3 Regulation of gene repair and transcription in normal human cells, and in premature aging syndromes

1997 ◽  
Vol 379 (1) ◽  
pp. S41
Author(s):  
Vilhelm A. Bohr ◽  
Adayabalam Balajce ◽  
Grigory Dianov ◽  
Amrita Machwe ◽  
Alfred May ◽  
...  
Keyword(s):  
Human Cells ◽  
Premature Aging ◽  
Gene Repair ◽  
Normal Human ◽  
Normal Human Cells ◽  
Premature Aging Syndromes

scholarly journals Nuclear matrix, nuclear envelope and premature aging syndromes in a translational research perspective

2014 ◽  
Vol 29 ◽  
pp. 125-147 ◽  
Author(s):  
Pierre Cau ◽  
Claire Navarro ◽  
Karim Harhouri ◽  
Patrice Roll ◽  
Sabine Sigaudy ◽  
...  
Keyword(s):  
Nuclear Envelope ◽  
Translational Research ◽  
Nuclear Matrix ◽  
Premature Aging ◽  
Research Perspective ◽  
Premature Aging Syndromes

scholarly journals THE ACTIVITY OF APOPTOSIS AND PREMATURE AGING IN YOUNGAND MIDDLE-AGED MAN WITH POLYMORBID CARDIOVASCULAR DISEASEAND NON-PSYCHOTIC MENTAL DISORDERS

2017 ◽  
Vol 9 (1) ◽  
pp. 48-53
Author(s):  
A S Partsernyak ◽  
M A Aflitonov ◽  
Y Sh Khalimov ◽  
E B Kireeva ◽  
A N Mironenko ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Protein Level ◽  
Standard Therapy ◽  
P53 Protein ◽  
Test Methods ◽  
Functional Class ◽  
Premature Aging ◽  
Control Group ◽  
Second Phase ◽  
The Third

Objective: To study the activity of apoptosis and premature aging in individuals of middle age with polymorbidity cardiovascular disease and non-psychotic mental disorders.Design and methods: The study included 78 men with MCVP and 20 healthy men. used in the study: complex psychological test methods and laboratory-instrumental evaluation of the cardiovascular system. definition p53 protein was performed by ELISA using kits BMS eBioscience BMS256 (BenderMedSys- tems, uSA). Results: n the group of patients with polymorbidity cardiovascular disease (PTS) of the p53 protein level was 4,89 uI / ml in the control group, p53 0,93 uI / ml. In all groups celebrated the acceler- ated pace of aging by an average of 10 years, compared with the control group. In the second phase of the study, patients were divided into three groups, depending on the planned treatment scheme. In the group of patients treated with standard therapy of p53 protein level was 3,51 uI / ml, from the group comprising in addition to standard therapy, psychotherapy - 2,34 uI / ml, in the third group, where the methodology of psycho-physiological and psychological visual and auditory correction - 1 8 uI / ml. After a course of treatment in all groups showed slowing premature aging . The first and second groups , a transition of V in class IV , the third group III to V of the functional class of aging . during the correlation analysis it was found a strong correlation between p53 protein and BV (r + 0,69; p < 0.05).Conclusions: Patients with polymorbidity cardiovascular disease marked increase in titer of apop- tosis protein p53 , accelerating premature aging 7-10 years. A direct correlation between p53 protein and biological age (r + 0,69; p < 0.05). Against the background of complex treatment with standard therapy with psycho-physiological and psychological visual and auditory correction decreased prema- ture aging, as compared with the groups that used the standard therapy for 8-10 years.

scholarly journals PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Olivia Cypris ◽  
Monika Eipel ◽  
Julia Franzen ◽  
Corinna Rösseler ◽  
Vithurithra Tharmapalan ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Bone Marrow ◽  
Neuronal Differentiation ◽  
Bone Marrow Failure ◽  
Premature Aging ◽  
Telomere Attrition ◽  
Bone Marrow Failure Syndromes ◽  
Epigenetic Age ◽  
Premature Aging Syndromes ◽  
Aberrant Dna Methylation

Abstract Background Dyskeratosis congenita (DKC) and idiopathic aplastic anemia (AA) are bone marrow failure syndromes that share characteristics of premature aging with severe telomere attrition. Aging is also reflected by DNA methylation changes, which can be utilized to predict donor age. There is evidence that such epigenetic age predictions are accelerated in premature aging syndromes, but it is yet unclear how this is related to telomere length. DNA methylation analysis may support diagnosis of DKC and AA, which still remains a challenge for these rare diseases. Results In this study, we analyzed blood samples of 70 AA and 18 DKC patients to demonstrate that their epigenetic age predictions are overall increased, albeit not directly correlated with telomere length. Aberrant DNA methylation was observed in the gene PRDM8 in DKC and AA as well as in other diseases with premature aging phenotype, such as Down syndrome and Hutchinson-Gilford-Progeria syndrome. Aberrant DNA methylation patterns were particularly found within subsets of cell populations in DKC and AA samples as measured with barcoded bisulfite amplicon sequencing (BBA-seq). To gain insight into the functional relevance of PRDM8, we used CRISPR/Cas9 technology to generate induced pluripotent stem cells (iPSCs) with heterozygous and homozygous knockout. Loss of PRDM8 impaired hematopoietic and neuronal differentiation of iPSCs, even in the heterozygous knockout clone, but it did not impact on epigenetic age. Conclusion Taken together, our results demonstrate that epigenetic aging is accelerated in DKC and AA, independent from telomere attrition. Furthermore, aberrant DNA methylation in PRDM8 provides another biomarker for bone marrow failure syndromes and modulation of this gene in cellular subsets may be related to the hematopoietic and neuronal phenotypes observed in premature aging syndromes. Graphical abstract

Genodermatoses with Premature Aging/Syndromes

2015 ◽  
pp. 1-19
Author(s):  
Adele Chedraoui ◽  
Abdul Ghani Kibbi ◽  
Mazen Kurban
Keyword(s):  
Premature Aging ◽  
Premature Aging Syndromes
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