Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Environment-dependent striatal gene expression in the BACHD rat model for Huntington disease

ABSTRACT: We examined effects of early life stress (ELS) and environmental enrichment (EE) during development on BACHD rat striatal gene expression using RNA sequencing

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE107259 | GEO | 2018/04/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Environment-dependent striatal gene expression in the BACHD rat model for Huntington disease

Project description:Environment-dependent striatal gene expression in the BACHD rat model for Huntington disease

| PRJNA419484 | ENA

Environment-dependent striatal gene expression in the BACHD rat model for Huntington disease.

Project description: Not available

| S-EPMC5895842 | biostudies-other

The BACHD Rat Model of Huntington Disease Shows Signs of Fronto-Striatal Dysfunction in Two Operant Conditioning Tests of Short-Term Memory.

Project description: Not available

| S-EPMC5207398 | biostudies-literature

A novel BACHD transgenic rat exhibits characteristic neuropathological features of Huntington disease.

Project description: Not available

| S-EPMC6621569 | biostudies-literature

Cardiac fibrosis in the BACHD mouse model of Huntingtonâs Disease

Project description:Aims: While Huntingtonâs disease is classified as a neurological disorder, HD patients exhibit a high incidence of cardiovascular events leading to heart failure and death. In this study, we sought to better understand the cardiovascular phenotype of HD using the BACHD mouse model. Methods and Results: The age-related decline in cardiovascular function was assessed by echocardiograms, electrocardiograms, histological and microarray analysis. We found that structural and functional differences between WT and BACHD hearts start at 3mo of age and continue throughout life. The aged BACHD mice develop cardiac fibrosis. The BACHD mice exhibited adaptive physiological changes to chronic isoproterenol challenge; however, the treatment exacerbated fibrotic lesions in the heart. Gene expression analysis indicates a strong tilt toward apoptosis in the young mutant tissue as well as changes in genes involved in cellular metabolism and proliferation. With age, the number of genes with altered expression increased with the largest changes occurring in the cardiovascular disease and cellular metabolism clusters. Conclusions: The BACHD model of HD exhibit a number of changes in cardiovascular function that start early in the disease progress and may provide an explanation for the higher CV risk in HD. These changes are consistent with dysfunction in ANS regulation although the hearts did respond adaptively to Î²-adrenergic challenge. Gene expression pattern changes are subtle but suggests biomarkers focusing on apoptosis, metabolism, immune function are worth further exploration. Microarray-based gene expression analysis in tissue from transgenic mice and controls at different ages

2016-03-01 | E-GEOD-76593 | biostudies-arrayexpress

Cardiac fibrosis in the BACHD mouse model of Huntington’s Disease

Project description:Aims: While Huntington’s disease is classified as a neurological disorder, HD patients exhibit a high incidence of cardiovascular events leading to heart failure and death. In this study, we sought to better understand the cardiovascular phenotype of HD using the BACHD mouse model. Methods and Results: The age-related decline in cardiovascular function was assessed by echocardiograms, electrocardiograms, histological and microarray analysis. We found that structural and functional differences between WT and BACHD hearts start at 3mo of age and continue throughout life. The aged BACHD mice develop cardiac fibrosis. The BACHD mice exhibited adaptive physiological changes to chronic isoproterenol challenge; however, the treatment exacerbated fibrotic lesions in the heart. Gene expression analysis indicates a strong tilt toward apoptosis in the young mutant tissue as well as changes in genes involved in cellular metabolism and proliferation. With age, the number of genes with altered expression increased with the largest changes occurring in the cardiovascular disease and cellular metabolism clusters. Conclusions: The BACHD model of HD exhibit a number of changes in cardiovascular function that start early in the disease progress and may provide an explanation for the higher CV risk in HD. These changes are consistent with dysfunction in ANS regulation although the hearts did respond adaptively to β-adrenergic challenge. Gene expression pattern changes are subtle but suggests biomarkers focusing on apoptosis, metabolism, immune function are worth further exploration.

2016-03-01 | GSE76593 | GEO

Foxp2 Overexpression in BACHD mice

Project description:Foxp2 Overexpression in BACHD mice

| PRJNA414379 | ENA

Striatal proteomics of CMS-treated rats

Project description:We used a chronic mild stress (CMS) protocol to separate susceptible-depression, susceptible-anxiety and insusceptible rat subgroups. Differential proteomes in the striatal were analyzed based on isobaric tags for relative and absolute quantitation (iTRAQ) labeling combined with mass spectrometry.

2021-05-19 | PXD026107 | iProX

The BACHD Rat Model of Huntington Disease Shows Specific Deficits in a Test Battery of Motor Function.

Project description: Not available

| S-EPMC5675855 | biostudies-literature

Transcription profiling of rat aortic and endocardial endothelial cells

Project description:Endocardial (EE) and Aortic (AE) endothelial cells were isolated from the same two rats, pooled (EE and AE kept separately) and cultured for 2 passages. Culture conditions and confluence of EE and AE cell cultures were kept as identical as possible. RNA was isolated and the expression profile of both endothelial cell types was compared using the Affymetrix rat genome U34A array.

2008-06-11 | E-GEOD-1478 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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