Chromatin footprints after double-hit stress
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE200670 | GEO | 2022/06/20
REPOSITORIES: GEO
Similar Datasets
Project description:Chromatin footprints after double-hit stress
| PRJNA825824 | ENA
Project description:Purpose: The goal of this study was to characterize molecular stress responses on transcriptional level in dorsal and ventral hippocampus separately. Methods: mRNA profiles of whole, dorsal and ventral hippocampus of mice 45min after first exposure to different acute stressors. The stressors were novelty (6min novel environment), restraint (30min immobilization), or cold swim (6min in 18 degree Celcius water). 5 mice were used per condition, using Illumina HiSeq4000. The sequence reads that passed quality filters were mapped with STAR, counted with RSEM and differential gene expression was calculated using the bioconducter package edgeR. Results: With our workflow, we identified 13902 genes per sample. Approximately 20% of the genes were differentially expressed between dorsal and ventral hippocampus at baseline, with a log2 fold change >±0.3 and p value <0.005. Approximately 100 genes are differentially expressed upon stress treatment in the whole hippocampus. If ventral and dorsal hippocampus were analyzed separately, numbers increased to 150 and 250 respectively. Stress-responsive genes vary between dorsal and ventral hippocampus, and also vary between different stressors. Further analysis identified a functional epigenetic gene cluster specific for the stress response in the ventral hippocampus. Conclusions: Our study represents the first RNA-seq analysis of dorsal and ventral hippocampus after different acute stress exposures.
2018-02-08 | GSE100236 | GEO
Project description:The acute stress response mobilizes energy to meet situational demands and re-establish homeostasis. Here, we used a brief forced swim exposure to trigger a strong stress response in mice. Using multiomic profiling we characterize the stress-induced molecular events in the dorsal (dHC) and ventral (vHC) hippocampus over time, across molecular scales, and down to the level of cell types and single cells.
2021-03-25 | GSE169509 | GEO
Project description:The acute stress response mobilizes energy to meet situational demands and re-establish homeostasis. Here, we used a brief forced swim exposure to trigger a strong stress response in mice. Using multiomic profiling we characterize the stress-induced molecular events in the dorsal (dHC) and ventral (vHC) hippocampus over time, across molecular scales, and down to the level of cell types and single cells.
2021-03-25 | GSE169510 | GEO
Project description:The acute stress response mobilizes energy to meet situational demands and re-establish homeostasis. Here, we used a brief forced swim exposure to trigger a strong stress response in mice. Using multiomic profiling we characterize the stress-induced molecular events in the dorsal (dHC) and ventral (vHC) hippocampus over time, across molecular scales, and down to the level of cell types and single cells.
2021-03-25 | GSE169505 | GEO
Project description:The hippocampus - one of the most studied brain regions – is a key target of the stress response and vulnerable to the detrimental effects of stress. Although its intrinsic organization is highly conserved throughout its long dorsal-ventral axis, the dorsal hippocampus is linked to spatial navigation and memory formation, whereas the ventral hippocampus is linked to emotional regulation. Here, we provide the first combined transcriptomic and proteomic profiling that reveals striking differences between dorsal and ventral hippocampus. Using various acute stress challenges we demonstrate that both regions display very distinct molecular responses, and that the ventral hippocampus is particularly responsive to the effects of stress. We demonstrate that separately analyzing dorsal and ventral hippocampus greatly increases the ability to detect region-specific stress effects, and we identify an epigenetic network, which is specifically sensitive to acute stress in the ventral hippocampus.
2019-10-03 | PXD006781 | Pride
Project description:Clarke2000 - One-hit model of cell death in
neuronal degenerations
This one-hit model fits different
neuronal-death associated diseases for different animal
models.
This model is described in the article:
A one-hit model of cell
death in inherited neuronal degenerations.
Clarke G, Collins RA, Leavitt BR,
Andrews DF, Hayden MR, Lumsden CJ, McInnes RR.
Nature 2000 Jul; 406(6792):
195-199
Abstract:
In genetic disorders associated with premature neuronal
death, symptoms may not appear for years or decades. This delay
in clinical onset is often assumed to reflect the occurrence of
age-dependent cumulative damage. For example, it has been
suggested that oxidative stress disrupts metabolism in
neurological degenerative disorders by the cumulative damage of
essential macromolecules. A prediction of the cumulative damage
hypothesis is that the probability of cell death will increase
over time. Here we show in contrast that the kinetics of
neuronal death in 12 models of photoreceptor degeneration,
hippocampal neurons undergoing excitotoxic cell death, a mouse
model of cerebellar degeneration and Parkinson's and
Huntington's diseases are all exponential and better explained
by mathematical models in which the risk of cell death remains
constant or decreases exponentially with age. These kinetics
argue against the cumulative damage hypothesis; instead, the
time of death of any neuron is random. Our findings are most
simply accommodated by a 'one-hit' biochemical model in which
mutation imposes a mutant steady state on the neuron and a
single event randomly initiates cell death. This model appears
to be common to many forms of neurodegeneration and has
implications for therapeutic strategies.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000538.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2014-08-07 | BIOMD0000000538 | BioModels
Project description:Acute stress provides many beneficial effects whereas chronic stress contributes to a variety of human health problems. The objective of this study was to use a rodent model to uncover hippocampal gene signatures associated with prolonged chronic stress which could potentially serve as biomarkers and therapeutic targets for early diagnosis and pharmacological intervention for stress induced disease. Mice were subjected to restraint stress over 7 consecutive days and gene expression changes in the hippocampus were analyzed at 3, 12 and 24 hours following the final restraint treatment. Data indicated that mice exposed to chronic restraint stress exhibit a differential gene expression profile compared to non-stressed controls. The greatest differences were observed 12 and 24 hrs following the final stress test.
2016-11-02 | E-MTAB-2402 | biostudies-arrayexpress
Project description:Aldh1l1CreERT2-RiboTag mice were used to purify and sequence astrocyte actively translated mRNAs from acute stress mouse models (20 minute forced swim) and non stressed controls.
2020-03-13 | GSE126172 | GEO
Project description:It was our goal to discern the genomic signatures of the ventral hippocampus, in male mice after exposure to exogenous corticosterone, an animal model that induces a blunted response to stress. In addition to wildtype mice, we used mice heterozygous for the single nucleotide polymorphism of the gene encoding for brain-derived neurotrophic factor, BDNF Val66Met, a mouse model that shows susceptibility to stress.
2021-05-19 | GSE174664 | GEO