Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Sex differences during acute myocarditis against coxsackievirus B3 (CVB3)-induced myocarditis (10 dpi) and chronic myocarditis/dilated cardiomyopathy (DCM) against CVB3-induced myocarditis (90 dpi)

ABSTRACT: Men are at an increased risk of dying from heart failure caused by inflammatory heart diseases such as atherosclerosis, myocarditis and dilated cardiomyopathy (DCM). We previously showed that immune responses in the heart are phenotypically distinct in male compared to female mice 10 days after infection resulting in severe DCM in males. Groups consisted of Infected Males, Infected Females, Uninfected Males and Uninfected females. There are 3 mice per group. A total of 12 samples were analyzed in this experiment (12 for 10 dpi and 12 for 90 dpi).

ORGANISM(S): Mus musculus

SUBMITTER: DeLisa Fairweather

PROVIDER: E-GEOD-35182 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

The study of sex differences during the innate immune response against coxsackievirus B3 (CVB3)-induced myocarditis (12hr post infection)

Project description:Men are at an increased risk of dying from heart failure caused by inflammatory heart diseases such as atherosclerosis, myocarditis and dilated cardiomyopathy (DCM). We previously showed that macrophages in the spleen are phenotypically distinct in male compared to female mice at 12 hours (h) after infection. This innate immune profile mirrors and predicts the cardiac immune response during acute myocarditis. Groups consisted of Infected Males, Infected Females, Uninfected Males and Uninfected females. There are 5 mice per group. A total of 20 samples were analyzed in this experiment.

2011-01-14 | E-GEOD-26630 | biostudies-arrayexpress

Sex differences during acute myocarditis against coxsackievirus B3 (CVB3)-induced myocarditis (10 dpi) and chronic myocarditis/dilated cardiomyopathy (DCM) against CVB3-induced myocarditis (90 dpi)

2012-01-19 | GSE35182 | GEO

Coxsackievirus B3 (CVB3) infection of AJ, B10.A, CSS3 and B6.chr3AJ (heart tissue day 4)

Project description:The pathogenesis of viral myocarditis is a multifactorial process involving host genetics, viral genetics and the environment in which they interact. Here, we used a model of infection with Coxsackievirus B3 to characterize the contribution of host genetics to viral myocarditis. We determined heart CVB3 load in mice from a classical intercross between progenitors A/J (H2a) and B10.A-H2a (B10.A) of different genetic backgrounds but with a common H2 haplotype. Here we compare whole genome expression patterns in infected and uninfected A/J and B10.A mice in order to determine which gene expression programs are common or distinct to each strain. Total RNA obtained from hearts of 3 AJ, 3 B10.A(H2a), 3 CSS3 and 3 B6.chr3AJ that were infected or uninfected with CVB3(CG) at 400pfu/g and collected at day 4 post infection.

2011-05-01 | E-GEOD-19496 | biostudies-arrayexpress

The study of sex differences during the innate immune response against coxsackievirus B3 (CVB3)-induced myocarditis (12hr post infection)

2011-01-14 | GSE26630 | GEO

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

Expression profiles of non-coding RNAs in the heart of mice with coxsackie B3 virus-induced myocarditis

Project description:Non-coding RNAs (ncRNAs) are critical regulators of viral infection and inflammatory responses. However, the roles of ncRNAs in acute myocarditis (AM)M) remain unclear.To identify ncRNAs involved in viral myocarditis pathogenesis by RNA-seq.

2021-08-16 | E-MTAB-10823 | biostudies-arrayexpress

Global phosphoproteomic profiling reveals perturbed signaling in a mouse model of dilated cardiomyopathy

Project description:Project Description(50 to 5000 characters):Phospholamban (PLN) plays a central role in Ca2+ homeostasis in cardiac myocytes through its regulation of the SERCA2A Ca2+ pump. An inherited mutation converting arginine residue 9 in PLN to cysteine (R9C) results in dilated cardiomyopathy (DCM) in both humans and transgenic mice, but the downstream signaling defects leading to heart failure are poorly understood. Here, we used precision tandem mass spectrometry to gain unbiased insights into the global phosphorylation dynamics of 2041 cardiac phosphoproteins in early affected heart tissue in the transgenic R9C mouse model of DCM compared to wild type littermates. 251 dysregulated phosphorylation sites were quantified after affinity capture and identification of 4337 phosphopeptides from fractionated whole heart homogenates. Enrichment analysis of the differential phosphoprotein patterns revealed dozens of signaling pathways regulating cardiovascular activity that are selectively impaired in early stages of DCM. Strikingly, dysregulated signaling through the Notch-1 receptor, recently linked to cardiomyogenesis and embryonic cardiac stem cell development and differentiation but never directly implicated in DCM before, was one of the most prominently perturbed pathways. We verified dysregulation of Notch1 downstream components in early symptomatic R9C transgenic mouse hearts compared to wild type by immunoblot analysis and confocal immunofluorescence microscopy. These data reveal unexpected connections between protein kinases, cell signaling networks and downstream effectors essential for proper cardiac function

2016-12-12 | PXD004810 | Pride

Dilated cardiomyopathy vs Myocarditis

Project description:Sequencing data of biopsies from Myocarditis and DCM patients

2018-09-28 | GSE120567 | GEO

Transcription profiling of mice hearts comparing microRNA-22 overexpression to wildtype

Project description:To explore the role of miR-22 in the heart, we generated miR-22 null and transgenic mice. Cardiac transgenic overexpression of miR-22 in vivo led to cardiac hypertrophy that evolved into progressive dilated cardiomyopathy (DCM) in unstressed hearts. We found that miR-22 directly regulates two transcriptional antagonists, purine rich element binding protein B (PURB), a repressor, and serum response factor (SRF), an activator, in the heart. Through these gain- and loss-of-function experiments in mice, we suggest that a primary function of miR-22 is to fine tune the relative expression and activity of these two transcriptional antagonists to influence contractile gene expression, function, growth and adaptation of the heart to stress.

2012-12-01 | E-MTAB-501 | biostudies-arrayexpress

STAT3 Suppresses Cardiomyocytes Apoptosis in CVB3-Induced Myocarditis Via Survivin.

Project description:Background: Viral myocarditis (VMC) is a common inflammatory cardiovascular disease with unclear mechanisms, which mainly affects children and adolescents. Apoptosis is the key to CVB3-induced myocarditis, and blocking this process may be beneficial to the therapy of VMC. Hence, this study aimed to explore the protective function of STAT3 on cardiomyocyte apoptosis of VMC and its underlying mechanisms. Methods and Results: In this research, we confirmed that STAT3 was significantly activated in both animal and cell models of VMC. To further clarify what role did STAT3 play in VMC, AG490, an inhibitor of STAT3, was used to suppress p-STAT3. Our results demonstrated that decreased expression of p-STAT3 caused by AG490 significantly aggravated severity of VMC with elevated myocardial inflammation, deteriorative ventricular systolic function and increased mortality. It suggested that STAT3 plays a protective role in VMC. To further identify the anti-apoptosis impact that activated STAT3 made, we constructed lentivirus to regulate the expression of STAT3 in NMCs. We found that up-regulated activated STAT3 attenuated cardiomyocyte apoptosis, but down-regulated one aggravated that, which verified activated STAT3 played an anti-apoptosis role in VMC. Following that, we explored what elements are involved in the anti-apoptotic mechanism of activated STAT3 by using survivin inhibitor YM155. The result showed the anti-apoptotic effect of activated STAT3 does not work in the case of survivin inhibition. Conclusion: Our findings demonstrated STAT3 by targeting survivin alleviated cardiomyocyte apoptosis in CVB3-induced myocarditis.

| S-EPMC7919905 | biostudies-literature

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