Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome profiling of spleen, blood and hemi-brain of social stressed C57B6 mice exhibiting PTSD like features

ABSTRACT: Social stress mouse models were used to simulate human post-traumatic stress disorder (PTSD). C57B/6 mice exposed to SJL aggressor mice exhibited behaviors accepted as PTSD-in-mouse phenotype: 'frozen' motion, aggressor's barrier avoidance, startled jumping, and retarded locomotion. Transcripts in spleen, blood and hemi-brain of stressed and control C57B/6 mice were analyzed using Agilent's mouse genome-wide arrays.

ORGANISM(S): Mus musculus

PROVIDER: GSE68076 | GEO | 2015/12/31

SECONDARY ACCESSION(S): PRJNA281668

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome profiling of spleen, blood and hemi-brain of social stressed C57B6 mice exhibiting PTSD like features

Project description:Social stress mouse models were used to simulate human post-traumatic stress disorder (PTSD). C57B/6 mice exposed to SJL aggressor mice exhibited behaviors accepted as PTSD-in-mouse phenotype: 'frozen' motion, aggressor's barrier avoidance, startled jumping, and retarded locomotion. Transcripts in spleen, blood and hemi-brain of stressed and control C57B/6 mice were analyzed using Agilent's mouse genome-wide arrays. C57B6 mice were exposed to SJL aggressor mice for periods of 5 days and 10 days (6 hours each day) to induce anxiety/stress which parallels to PTSD in human. Organs, blood and brain regions were collected after 24 hours and 1.5 week of post 5 days social defeat period; and 24 hour and 6 weeks post 10 days social stress period.

2015-12-31 | E-GEOD-68076 | biostudies-arrayexpress

Brain transcriptome profiles in mouse model simulating features of post-traumatic stress disorder

2015-04-20 | GSE45035 | GEO

Brain transcriptome profiles in mouse model simulating features of post-traumatic stress disorder

Project description:Social stress mouse models were used to simulate human post-traumatic stress disorder (PTSD). C57B/6 mice exposed to SJL aggressor mice exhibited behaviors accepted as PTSD-in-mouse phenotype: 'frozen' motion, aggressor’s barrier avoidance, startled jumping, and retarded locomotion. Transcripts in hippocampus, amygdala, medial prefrontal cortex, ventral striatum (nucleus acumbens), septal region, corpus striatum, hemi-brain, blood, spleen and heart of stressed and control C57B/6 mice were analyzed using Agilent’s mouse genome-wide arrays. C57B6 mice were exposed to SJL aggressor mice for periods of 5 days and 10days (6 hours each day) to induce anxiety/stress which parallels to PTSD in human Organs, blood and brain regions were collected after 24 hours and 1.5 week of post 5 days social defeat period; and 24 hour and 6 weeks post 10 days social stress period.

2015-04-20 | E-GEOD-45035 | biostudies-arrayexpress

Molecular indicators of stress-induced neuroinflammation in a mouse model simulating features of post-traumatic stress disorder

Project description:A social-stress mouse model, involving exposure of an intruder (male C57BL/6) mouse to a resident aggressor (male SJL) mouse followed by exposure to trauma reminders with post-trauma periods, was used to simulate features of human PTSD. Transcriptome changes in blood, brain regions and spleen, and DNA methylome changes in hemi-brain of aggressor-exposed and control C57BL/6 mice were assayed at one, 10 and 42 days of post-trauma periods. Assessments of activation patterns for differentially expressed transcripts (overlapping among hemi-brain, blood and spleen), and differentially methylated promoter regions showed increased activations of inflammatory pathways, and inhibited pathways related to neurogenesis and synaptic plasticity at longer post-trauma days. In amygdala, hippocampus and medial pre-frontal cortext, these pathways were activated at earlier post-trauma periods. But at longer post-trauma periods, neurogenesis and synaptic plasticity were inhibited while lower level of activated inflammation persisted in hippocampus and medial pre-frontal cortex. Pathways implicated in diabetes, insulin signaling, metabolic disorder, mitochondrial dysfunctions, circadian disruption, oxidative stress and inhibited telomere maintenance were significantly enriched. Identification of brain – blood overlapping molecular signatures provide increased confidence in using blood as brain surrogate sample for clinical translation. Our findings suggest that stress-induced inflammation triggers impaired neurogenesis, cognitive decline, and chronic pain (physical complaints in PTSD patients). Signaling pathways implicated in neurogenesis and synaptic plasticity seem to be mediating the effect of neuroinflammation in the development and maintenance of behavioral manifestations of PTSD. While inflammation seems to be directly involved in tissue damage triggering, exacerbating or maintaining the somatic comorbid pathologies of PTSD.

2017-08-31 | GSE85495 | GEO

Gene expression signatures in heart tissues of mice simulating posttraumatic stress disorder (PTSD) [Study2]

2013-12-04 | E-GEOD-52871 | biostudies-arrayexpress

miRNA expression signatures in heart tissues of mice simulating posttraumatic stress disorder (PTSD) [Study1]

2013-12-04 | E-GEOD-52869 | biostudies-arrayexpress

Gene expression signatures in heart tissues of mice simulating posttraumatic stress disorder (PTSD) [Study1]

2013-12-04 | E-GEOD-52866 | biostudies-arrayexpress

miRNA expression signatures in heart tissues of mice simulating posttraumatic stress disorder (PTSD) [Study2]

Project description:Using a PTSD mouse model, we investigated the longitudinal transcriptomic changes in heart tissues after the exposure to stress through intimidation We designed our time-course study (Study II) with three experimental conditions where we varied the length of time that subservient mice were exposed to aggressor mice with the same length of rest time after the exposure (1day). The conditions included were 1day-exposure (T1R1), 2day-exposure (T2R1) and 3day-exposure (T3R1). We designed our initial study (Study I) with four experimental conditions where we varied the length of time that subservient mice were exposed to aggressor mice and the length of rest time after the exposure. The conditions included were short exposure-short rest (T5R1-T indicates the number of days of trauma exposure; R indicates the number of days of rest after exposure), short exposure-long rest (T5R10), long exposure-short rest (T10R1) and long exposure-long rest (T10R42)

2013-12-04 | E-GEOD-52872 | biostudies-arrayexpress

PTSD mouse amygdala proteome

Project description:Posttraumatic stress disorder (PTSD) is a prevalent psychiatric disorder. Several studies have attempted to characterize molecular alterations associated with PTSD, but most findings were limited to the investigation of specific cellular markers in the periphery or defined brain regions. In the current study, we aimed to unravel affected molecular pathways/mechanisms in the fear circuitry associated with PTSD. We interrogated a foot shock induced-PTSD mouse model by integrating proteomics and metabolomics profiling data. Alterations at the proteome level were analyzed using in vivo 15N metabolic labeling combined with mass spectrometry in prelimbic cortex (PrL), anterior cingulate cortex (ACC), basolateral amygdala (BLA), central nucleus of amygdala (CeA) and CA1 of hippocampus between shocked and non-shocked (control) mice, with and without fluoxetine treatment.

2022-02-28 | PXD002288 | Pride

PTSD mouse anterior cingulate cortex proteome

Project description:Posttraumatic stress disorder (PTSD) is a prevalent psychiatric disorder. Several studies have attempted to characterize molecular alterations associated with PTSD, but most findings were limited to the investigation of specific cellular markers in the periphery or defined brain regions. In the current study, we aimed to unravel affected molecular pathways/mechanisms in the fear circuitry associated with PTSD. We interrogated a foot shock induced PTSD mouse model by integrating proteomics and metabolomics profiling data. Alterations at the proteome level were analyzed using in vivo 15N metabolic labeling combined with mass spectrometry in prelimbic cortex (PrL), anterior cingulate cortex (ACC), basolateral amygdala (BLA), central nucleus of amygdala (CeA) and CA1 of hippocampus between shocked and non-shocked (control) mice, with and without fluoxetine treatment.

2018-10-17 | PXD002271 | Pride

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