Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genomic instability in the naturally and prematurely aged myocardium [variants: data set 1]

ABSTRACT: Our data demonstrate that genomic instability does not evidently contribute to naturally aging of the mouse heart and support the contention that the endogenous DNA repair machinery is remarkably active to maintain genomic integrity in cardiac cells throughout life.

ORGANISM(S): Mus musculus

PROVIDER: GSE124083 | GEO | 2021/09/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genomic instability in the naturally and prematurely aged myocardium [variants: data set 2]

Project description:Our data demonstrate that genomic instability does not evidently contribute to naturally aging of the mouse heart and support the contention that the endogenous DNA repair machinery is remarkably active to maintain genomic integrity in cardiac cells throughout life.

2021-09-15 | GSE129278 | GEO

Genomic instability in the naturally and prematurely aged myocardium [RNA-Seq]

2021-09-15 | GSE124005 | GEO

Genomic instability in the naturally and prematurely aged myocardium

Project description:Genomic instability in the naturally and prematurely aged myocardium

| PRJNA510744 | ENA

Genomic instability in the naturally and prematurely aged myocardium [variants: data set 2]

Project description:Genomic instability in the naturally and prematurely aged myocardium [variants: data set 2]

| PRJNA530713 | ENA

Genomic instability in the naturally and prematurely aged myocardium [variants: data set 1]

Project description:Genomic instability in the naturally and prematurely aged myocardium [variants: data set 1]

| PRJNA510748 | ENA

Genomic instability in the naturally and prematurely aged myocardium [RNA-Seq]

Project description:Genomic instability in the naturally and prematurely aged myocardium [RNA-Seq]

| PRJNA510746 | ENA

Genomic instability in the naturally and prematurely aged myocardium

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-09-15 | GSE124087 | GEO

DNA damage in normally and prematurely aged mice.

Project description:Steady-state levels of spontaneous DNA damage, the by-product of normal metabolism and environmental exposure, are controlled by DNA repair pathways. Incomplete repair or an age-related increase in damage production and/or decline in repair could lead to an accumulation of DNA damage, increasing mutation rate, affecting transcription, and/or activating programmed cell death or senescence. These consequences of DNA damage metabolism are highly conserved, and the accumulation of lesions in the DNA of the genome could therefore provide a universal cause of aging. An important corollary of this hypothesis is that defects in DNA repair cause both premature aging and accelerated DNA damage accumulation. While the former has been well-documented, the reliable quantification of the various lesions thought to accumulate in DNA during aging has been a challenge. Here, we quantified inhibition of long-distance PCR as a measure of DNA damage in liver and brain of both normal and prematurely aging, DNA repair defective mice. The results indicate a marginal, but statistically significant, increase in spontaneous DNA damage with age in normal mouse liver but not in brain. Increased levels of DNA damage were not observed in the DNA repair defective mice. We also show that oxidative lesions do not increase with age. These results indicate that neither normal nor premature aging is accompanied by a dramatic increase in DNA damage. This suggests that factors other than DNA damage per se, for example, cellular responses to DNA damage, are responsible for the aging phenotype in mice.

| S-EPMC3655155 | biostudies-literature

Interleukin-6 neutralization ameliorates symptoms in prematurely aged mice.

Project description:Hutchinson-Gilford progeria syndrome (HGPS) causes premature aging in children, with adipose tissue, skin and bone deterioration, and cardiovascular impairment. In HGPS cells and mouse models, high levels of interleukin-6, an inflammatory cytokine linked to aging processes, have been detected. Here, we show that inhibition of interleukin-6 activity by tocilizumab, a neutralizing antibody raised against interleukin-6 receptors, counteracts progeroid features in both HGPS fibroblasts and LmnaG609G / G609G progeroid mice. Tocilizumab treatment limits the accumulation of progerin, the toxic protein produced in HGPS cells, rescues nuclear envelope and chromatin abnormalities, and attenuates the hyperactivated DNA damage response. In vivo administration of tocilizumab reduces aortic lesions and adipose tissue dystrophy, delays the onset of lipodystrophy and kyphosis, avoids motor impairment, and preserves a good quality of life in progeroid mice. This work identifies tocilizumab as a valuable tool in HGPS therapy and, speculatively, in the treatment of a variety of aging-related disorders.

| S-EPMC7811841 | biostudies-literature

Theophylline derivatives promote the activation of primordial follicles and ameliorate fertility deficits in naturally aged mice

Project description:The residual dormant primordial follicles in aged women and patients with premature ovarian insufficiency (POI) are difficult to activate in vivo. In this study, we found that PDE1A, PDE2A and PDE6D were expressed mainly in mouse primordial follicle oocytes and that PDE1A and PDE2A levels were significantly decreased during the activation of primordial follicles. The specific inhibitors of PDE1 (nimodipine), PDE2 (EHNA) and PDE5/6 (zaprinast) and the nonspecific PDE inhibitors theophylline derivatives (including aminophylline, dyphylline, enprofylline, choline theophyllinate, doxofylline, arofylline and lisofylline) activated mouse primordial follicles. These inhibitors also increased the levels of cyclic adenosine monophosphate (cAMP) and phosphorylated protein kinase B (p-Akt) in cultured mouse ovaries. Moreover, the administration of aminophylline, dyphylline and enprofylline to neonatal mice by intraperitoneal injection and to adolescent mice by oral treatment increased the number of growing follicle and the levels of p-Akt in the ovaries. Importantly, the oral administration of aminophylline increased the quantity and quality of ovulated oocytes and the number of offspring in naturally aged mice. In addition, aminophylline, dyphylline and enprofylline activated human primordial follicles and increased p-Akt levels. Thus, theophylline derivatives activate primordial follicles by increasing cAMP levels and activating the PI3K/Akt pathway, and the oral administration of aminophylline increases fertility in naturally aged female mice. As oral medications, theophylline derivatives may be used to increase fertility in aged women and patients with POI.

2024-05-30 | GSE263843 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data