Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Senescence progression in the normal human fibroblast, WI-38 cells induced with plasma membrane damage, calcium influx, DNA damage and telomere shortening.

ABSTRACT: To investigate the comparison of senescence progression in plasma membrane damage-, calcium influx-, DNA damage- and telomere shortening-induced senescence in the normal human fibroblast cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE222400 | GEO | 2024/01/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Senescence progression in the normal human fibroblast, WI-38 cells induced with plasma membrane damage, calcium influx, DNA damage and telomere shortening.

Project description:Senescence progression in the normal human fibroblast, WI-38 cells induced with plasma membrane damage, calcium influx, DNA damage and telomere shortening.

| PRJNA921872 | ENA

Telomeric 8-Oxoguanine Drives Rapid Premature Senescence in the Absence of Telomere Shortening

Project description:Oxidative stress is a primary cause of cellular senescence and contributes to the pathogenesis of numerous human diseases. Oxidative damage to telomeric DNA is proposed to trigger premature senescence by accelerating telomere shortening. Here we tested this model directly using a precision tool to produce the common base lesion 8-oxoguanine (8oxoG) exclusively at telomeres in human fibroblast and epithelial cells. A single induction of telomeric 8oxoG is sufficient to trigger multiple hallmarks of p53-dependent senescence. Telomeric 8oxoG activates ATM and ATR signaling, and enriches for markers of telomere dysfunction in replicating, but not quiescent cells. Acute 8oxoG production fails to shorten telomeres, but rather generates fragile sites and delayed mitotic DNA synthesis at telomeres, indicative of impaired replication. Based on our results we propose that oxidative stress promotes rapid senescence by producing oxidative base lesions which drive replication-dependent telomere fragility and dysfunction in the absence of shortening and shelterin loss.

2022-05-26 | GSE175686 | GEO

Length-independent telomere damage drives cardiomyocyte senescence

Project description:Ageing is the biggest risk factor to cardiovascular health and is associated with increased incidence of cardiovascular disease. Cellular senescence, a process driven in part by telomere shortening has been implicated in age-related cardiac dysfunction. However, the role of cellular senescence and its underlying mechanisms in slowly dividing/post-mitotic cardiomyocytes is not understood.

2019-02-06 | GSE95822 | GEO

Telomere Shortening Impairs PGC Fate Decision

Project description:Telomere Shortening Impairs PGC Fate Decision

| PRJNA660792 | ENA

Transcriptomic datat of senescence WI-38 cell

Project description:Senescence in WI-38 cell context was induce by RASv12 over expression Cellular senescence is a permanent cell cycle arrest that is triggered by cancer- initiating or promoting events in mammalian cells and is now considered a major tumour suppressor mechanism. Here, we did a transcriptomic analysis and compared WI-38 contol wich is a human fibroblaste cell line and WI-38 that overexpressed RASv12 a G protein that induce senescence. The goal of our project is to compare transciptomic profile of human growing fibroblast (WI-38 control) and senescent human fibroblast (WI-38 OERAS)

2011-11-16 | GSE33710 | GEO

Transcriptomic datat of senescence WI-38 cell

2011-11-16 | E-GEOD-33710 | biostudies-arrayexpress

Microscopic heat pulse-induced calcium dynamics in single WI-38 fibroblasts.

Project description:Temperature-sensitive Ca(2+) dynamics occur primarily through transient receptor potential channels, but also by means of Ca(2+) channels and pumps on the endoplasmic reticulum membrane. As such, cytoplasmic Ca(2+) concentration ([Ca(2+)]cyt) is re-equilibrated by changes in ambient temperature. The present study investigated the effects of heat pulses (heating duration: 2 s or 150 s) on [Ca(2+)]cyt in single WI-38 fibroblasts, which are considered as normal cells. We found that Ca(2+) burst occurred immediately after short (2 s) heat pulse, which is similar to our previous report on HeLa cells, but with less thermosensitivity. The heat pulses originated from a focused 1455-nm infrared laser light were applied in the vicinity of cells under the optical microscope. Ca(2+) bursts induced by the heat pulse were suppressed by treating cells with inhibitors for sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA) or inositol trisphosphate receptor (IP3R). Long (150 s) heat pulses also induced Ca(2+) bursts after the onset of heating and immediately after re-cooling. Cells were more thermosensitive at physiological (37°C) than at room (25°C) temperature; however, at 37°C, cells were responsive at a higher temperature (ambient temperature+heat pulse). These results strongly suggest that the heat pulse-induced Ca(2+) burst is caused by a transient imbalance in Ca(2+) flow between SERCA and IP3R, and offer a potential new method for thermally controlling Ca(2+)-regulated cellular functions.

| S-EPMC4629654 | biostudies-literature

Telomere Shortening Impairs PGC Fate Decision [ATAC-seq]

Project description:Telomere Shortening Impairs PGC Fate Decision [ATAC-seq]

| PRJNA660789 | ENA

Telomere Shortening Impairs PGC Fate Decision [RNA-seq]

Project description:Telomere Shortening Impairs PGC Fate Decision [RNA-seq]

| PRJNA660794 | ENA

Telomeric 8-Oxoguanine Drives Rapid Premature Senescence in the Absence of Telomere Shortening

Project description:Telomeric 8-Oxoguanine Drives Rapid Premature Senescence in the Absence of Telomere Shortening

| PRJNA733186 | ENA