Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

5 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of coxsackie virus vs control infected male mice to investigate the effects of infection on cardiac function

ABSTRACT: Male, adolescent A/J mice (4-5 week old) were either infected (IP) with coxsackievirus B3 (CVB3; 105 pfu) or PBS. CVB3 is a cardiotropic virus which leads to cardiac inflammation and fibrosis within 9 days after IP injection. We wanted to know how the virus would impact long term cardiac function, and whether changes in cardiac function could be associated with cardiac transcriptional regulation. At days 3, 9 and 30 days post-infection, hearts were imaged with 2D echocardiography (Sonos 5500, Philips). Briefly, mice were anesthesized subcutaneously with ketamine (0.45mg/kg) and xylazine (0.03mg/kg). Mice were placed in a dorsal recumbency position and the following systolic and diastolic measurements were taken (N=5 heart beats) using an S-12 (12MHz; Sonos 5000, Philips) probe: parasternal long axis, and short axis at the level of the mitral valve and papillary muscles. Measurements were utilized for calculation of wall thickness and functional parameters. Then, heart tissues were flash frozen (N=4 mice/group except CVB3 infected 30 day samples N=2) for hybridization to Affymetrix MG U74Av2 arrays.

ORGANISM(S): Mus musculus

DISEASE(S): CVB3 infected

SUBMITTER: John Gosink

PROVIDER: E-GEOD-1457 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

CxVB3 infection and cardiac function

Project description:Male, adolescent A/J mice (4-5 week old) were either infected (IP) with coxsackievirus B3 (CVB3; 105 pfu) or PBS. CVB3 is a cardiotropic virus which leads to cardiac inflammation and fibrosis within 9 days after IP injection. We wanted to know how the virus would impact long term cardiac function, and whether changes in cardiac function could be associated with cardiac transcriptional regulation. At days 3, 9 and 30 days post-infection, hearts were imaged with 2D echocardiography (Sonos 5500, Philips). Briefly, mice were anesthesized subcutaneously with ketamine (0.45mg/kg) and xylazine (0.03mg/kg). Mice were placed in a dorsal recumbency position and the following systolic and diastolic measurements were taken (N=5 heart beats) using an S-12 (12MHz; Sonos 5000, Philips) probe: parasternal long axis, and short axis at the level of the mitral valve and papillary muscles. Measurements were utilized for calculation of wall thickness and functional parameters. Then, heart tissues were flash frozen (N=4 mice/group except CVB3 infected 30 day samples N=2) for hybridization to Affymetrix MG U74Av2 arrays. Keywords: time-course

2004-12-01 | GSE1457 | GEO

MicroRNA155 mediates adverse inflammation in acute viral myocarditis LNA-antimiR155 treatment

Project description:For microRNA knockdown in vivo, a 15-mer LNA-antimiR oligonucleotide targeting mmu-miR-155 or an LNA control was administered to male 4-week-old C3H mice intravenously at a dose of 25 mg/kg per injection at days 1, 4 and 6 post-CVB3 infection. Samples were taken at 6 days post infection.

2012-06-06 | E-MEXP-3395 | biostudies-arrayexpress

Transcriptional profile of injured hearts treated with the cholinesterase inhibitor pyridostigmine (PYR) at Day 5

Project description:It has been shown that acetylcholine has anti-inflammatory properties. The aim of this study is to investigate the role of acetylcholine in cardiac inflammation. We used the diphtheria toxin (DT)-cardiomyocyte ablation model (DTR model) (Lavine et al., 2014 - PNAS) to induce cardiac injury (DT, 2 days, 2.5µg/kg, IP). Beginning one week prior to DT injury, mice were treated with vehicle (PBS, phosphate buffered saline) or the cholinesterase inhibitor pyridostigmine (PYR, 3mg/kg, SQ). Hearts were harvested at Day 5 post-DT-injury. Here, we provide the transcriptional profile of wild-type/PBS, wild-type/PYR, DTR/PBS and DTR/PYR hearts.

2019-08-21 | GSE116988 | GEO

Next Generation Sequencing of DIO Liver steatosis DMSO vs NCT (HNF4a agonist)

Project description:Mice rendered obese with high fat diet were treated by IP injection with N-trans caffeoyltyramine (NCT) (200 mg/kg bid) for 14 days, followed by harvesting of the liver for analysis, including RNA isolation.

2021-04-17 | GSE172234 | GEO

Next Generation Sequencing of DIO intestine DMSO vs NCT (HNF4a agonist)

2021-06-18 | GSE178435 | GEO

Cannabinoid exposure in rat adolescence reprograms the initial behavioral, molecular, and epigenetic response to cocaine

Project description:This dataset includes ATAC-Seq and RNA-seq data from rat prefrontal cortex and/or nucleus accumbens (postnatal date, PND 61), as part of characterizing how the rat brain responds to its first encounter with cocaine (PND 60) with or without preexposure to the synthetic cannabinoid WIN 55,212-2 (WIN) during adolescence (PND 42-52). WIN was administered twice daily during the latter eleven consecutive days (2 mg/kg, 3 days; 4 mg/kg, 4 days; 8 mg/kg, 4 days) and, following a week of WIN abstinence, animals were IP challenged with cocaine (10 mg/kg). Brain dissections were performed 24 hours after the cocaine IP challenge.

2019-07-27 | GSE134935 | GEO

Untargeted_Sept_Nov_Carnitine_Study

Project description:4-week-old male mice were infected with 50,000 CL+luc parasites or remained uninfected. Urine was collected pre-infection and 4 days after infection. 7 days post infection, mice were treated with 0.06% carnitine in drinking water ad libitum or with benznidazole 100 mg/kg ip for 10 days. 17 days post infection, urine was collected and euthanized. Metabolites were extracted from urine in methanol and untargeted LCMS analysis ran on a Q Exactive plus instrument using a Phenomenex Luna Omega Polar C18 column.

2022-03-23 | MSV000089114 | MassIVE

Coxsackievirus B3 (CVB3) infection of 129S1 and 129X1 (heart tissue day 6)

Project description:We infected two strains of mice, 129S1/SvImJ and 129X1/SvJ, with coxsackievirus type b3 (CVB3) at a dose of 500 pfu/g. 129S1 mice developed increased cardiopathology despite equal viral replication. We hypothesized that the increased cardiopathology might result from an ongoing pathologic host response that we could characterize by global expression profiling. Gene expression was assessed in hearts from 129S1 and 129X1 mice that were uninfected or infected for 6 days. Total RNA obtained from hearts of 3 129S1 and 3 129X1 that were infected or uninfected with CVB3(H3) at 500pfu/g and collected at day 6 post infection

2013-04-01 | E-GEOD-44706 | biostudies-arrayexpress

Transcription profiling of rat heart from a spontaneously hypertensive strain treated with doxorubicin or dexrazoxane and then doxorubicin

Project description:This study was initiated to characterize early DOX-induced changes in cardiac gene expression in order to identify potential additional areas for clinical intervention. Male spontaneously hypertensive rats (SHR) received 3 mg/kg DOX or vehicle (iv) 30 minutes following pretreatment with 50 mg/kg DZR or saline (ip) weekly for 1, 2 or 3 weeks.

2009-06-01 | E-MEXP-2071 | biostudies-arrayexpress

Changes in the cardiac transcriptome following isoproterenol infusion and coadministration of minocycline

Project description:Adverse cardiac remodeling contributes to the development and progression of heart failure (HF) driven, in part, by inappropriate sympathetic nervous system activation. While blockade of β-adrenergic receptors (β-AR) is a common therapeutic strategy in HF, not all patients respond necessitating elucidation of additional therapeutic approaches. Minocycline is an FDA-approved antibiotic with pleiotropic properties, independent of its antimicrobial action, and recent evidence suggests it may act by altering gene expression via changes in miRNA expression. Therefore, we hypothesized that minocycline would prevent adverse cardiac remodeling induced by the β-AR agonist isoproterenol involving relevant alterations in the miRNA-mRNA transcriptome. Male C57BL/6J mice received Iso (30 mg/kg/d, sc) or vehicle for 21 days via osmotic minipump and daily treatment with either minocycline (50 mg/kg, ip) or sterile saline. Isoproterenol infusion induced cardiac hypertrophy, with no change in cardiac function, that was prevented by minocycline. Total mRNA sequencing revealed that isoproterenol altered gene networks associated with inflammation and metabolism while activation of fibrosis was predicted by integrated miRNA-mRNA sequencing, involving miR-21, -30a, -34a, -92a, and -150, among others. Conversely, the cardiac miRNA-mRNA transcriptome predicted inhibition of fibrosis in hearts from mice treated with minocycline plus isoproterenol involving anti-fibrotic shifts in Atf3 and Itgb6 gene expression associated with upregulation of miR-194. Consistent with these gene signatures, picrosirius red staining confirmed isoproterenol-induced cardiac fibrosis and that this was prevented by minocycline. These results demonstrate the therapeutic potential of minocycline to attenuate adverse cardiac remodeling via miRNA-mRNA-dependent mechanisms, especially related to reduced cardiac fibrosis.

2024-02-15 | GSE255532 | GEO

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