Chagas_Heart_Phosphoproteomics
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Orbitrap Fusion
ORGANISM(S): Trypanosoma Cruzi (ncbitaxon:5693) Mus Musculus (ncbitaxon:10090)
SUBMITTER: 
David Gonzalez
PROVIDER: MSV000084188 | MassIVE | Fri Aug 09 09:13:00 BST 2019
SECONDARY ACCESSION(S): PXD014969
REPOSITORIES: MassIVE
Similar Datasets
Project description:An efficient innate immune recognition of the intracellular parasite T. cruzi is crucial for host protection against development of Chagas disease, which often leads to multiple organ damage, particularly the heart leading to cardiomyopathy. Mechanisms modulated by MyD88 have been shown to be necessary for resistance against T, cruzi infection. Recently, Nod-like receptors have been shown to play an important role as innate immune sensors, particularly as they relate to inflammasome function, caspase activation, and inflammatory cytokine production. In this study, we aimed to investigate the participation of innate immune responses in general, and inflammasomes in particular, in heart inflammation and cardiac damage upon infection with the T. cruzi parasite. We used microarrays to gain insight into gene expression in the cardiac tissue of mice infected with the causative agent of Trypanosoma cruzi, and identified distinct classes of up-regulated genes during this process, including important genes involved in inflammasome activation and innate immune responses in general. The hearts of C57BL/6 mice day 18 post-infection with a Y strain of the parasite T. cruzi, and uninfected controls were extraced for RNA extraction and hybridization on Affymetrix microarrays. We sought to compare gene expression among two groups of mice, and so extracted the hearts of 3 control uninfected mice, and of 3 infected mice 18 days post-infection.
2012-11-20 | E-GEOD-41089 | biostudies-arrayexpress
Project description:Chronic chagasic cardiomyopathy is a leading cause of heart failure in Latin American countries. About 30% of Trypanosoma cruzi-infected individuals develop this severe symptomatic form of the disease, characterized by intense inflammatory response accompanied by fibrosis deposition in the heart. We performed a microarray analysis of a mouse model of this disease and identified >5% alterations of gene expression in the heart. Most of the upregulations were associated with immune-inflammatory responses (chemokines, adhesion molecules, cathepsins and MHC molecules) and fibrosis deposition (extracellular matrix components, lysyl oxidase and Timp1). Our results indicate potentially relevant factors involved in the pathogenesis of the disease that may provide new therapeutic targets in chronic Chagas’ disease.
2009-08-07 | GSE17363 | GEO
Project description:Trypanosoma cruzi infection is a major cause of cardiomyopathy. Gene profiling studies of hearts from infected mice have revealed prominent changes in gene expression within many functional pathways. This variety of transcriptomic changes in infected mice raises the question of whether gene expression alterations in whole hearts are due to changes in infected cardiac myocytes or other cells or even to systemic effects of the infection on the heart. We employed microarrays to examine infected cardiac myocyte cultures 48 hr post-infection. Statistical comparison of gene expression levels of 2,258 well annotated unigenes in four independent cultures of infected and uninfected myocytes detected (p < 0.05) significant > 1.5 absolute fold changes in 221 (8.8%) of the sampled genes. Major categories of affected genes included those involved in immune response, extracellular matrix and cell adhesion. While changes in extracellular matrix and cell adhesion genes were anticipated, modulation of immune response genes in the infected myocytes was surprising. These findings on infected cardiac myocytes in culture reveal that altered gene expression described in the heart in Chagas disease are the consequence of both direct infection of the myocytes and resulting from presence of other cell types in the myocardium and systemic effects of infection. Transcriptomic alteration in neonatal mouse cultured cardiomyocytes induced by the parasite T.cruzi were detected by profiling and compared using AECOM mouse 32k oligonucleotide arrays hybridized in the "multiple yellow" strategy described in Iacobas et al, Biochem Biophys Res Commun. 2006 349(1):329-38.
2010-05-15 | E-GEOD-17330 | biostudies-arrayexpress
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis).
2011-02-04 | GSE27054 | GEO
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis).
2011-02-17 | GSE27353 | GEO
Project description:An efficient innate immune recognition of the intracellular parasite T. cruzi is crucial for host protection against development of Chagas disease, which often leads to multiple organ damage, particularly the heart leading to cardiomyopathy. Mechanisms modulated by MyD88 have been shown to be necessary for resistance against T, cruzi infection. Recently, Nod-like receptors have been shown to play an important role as innate immune sensors, particularly as they relate to inflammasome function, caspase activation, and inflammatory cytokine production. In this study, we aimed to investigate the participation of innate immune responses in general, and inflammasomes in particular, in heart inflammation and cardiac damage upon infection with the T. cruzi parasite. We used microarrays to gain insight into gene expression in the cardiac tissue of mice infected with the causative agent of Trypanosoma cruzi, and identified distinct classes of up-regulated genes during this process, including important genes involved in inflammasome activation and innate immune responses in general.
2012-11-20 | GSE41089 | GEO
Project description:Trypanosoma cruzi infection is a major cause of cardiomyopathy. Gene profiling studies of hearts from infected mice have revealed prominent changes in gene expression within many functional pathways. This variety of transcriptomic changes in infected mice raises the question of whether gene expression alterations in whole hearts are due to changes in infected cardiac myocytes or other cells or even to systemic effects of the infection on the heart. We employed microarrays to examine infected cardiac myocyte cultures 48 hr post-infection. Statistical comparison of gene expression levels of 2,258 well annotated unigenes in four independent cultures of infected and uninfected myocytes detected (p < 0.05) significant > 1.5 absolute fold changes in 221 (8.8%) of the sampled genes. Major categories of affected genes included those involved in immune response, extracellular matrix and cell adhesion. While changes in extracellular matrix and cell adhesion genes were anticipated, modulation of immune response genes in the infected myocytes was surprising. These findings on infected cardiac myocytes in culture reveal that altered gene expression described in the heart in Chagas disease are the consequence of both direct infection of the myocytes and resulting from presence of other cell types in the myocardium and systemic effects of infection.
2009-08-04 | GSE17330 | GEO
Project description:Chronic chagasic cardiomyopathy is a leading cause of heart failure in Latin American countries. About 30% of Trypanosoma cruzi-infected individuals develop this severe symptomatic form of the disease, characterized by intense inflammatory response accompanied by fibrosis deposition in the heart. We performed a microarray analysis of a mouse model of this disease and identified >5% alterations of gene expression in the heart. Most of the upregulations were associated with immune-inflammatory responses (chemokines, adhesion molecules, cathepsins and MHC molecules) and fibrosis deposition (extracellular matrix components, lysyl oxidase and Timp1). Our results indicate potentially relevant factors involved in the pathogenesis of the disease that may provide new therapeutic targets in chronic Chagasâ disease. The heart transcriptomes of 4 age-mached Trypanosoma cruzi-infected and 4 control C57Bl/6 mice were profiled and compared using Duke Mouse 30k Oligonucleotide Arrays (Operon V3.0.1) hybridized in the "multiple yellow" strategy described in Iacobas et al, Biochem Biophys Res Commun. 2006 349(1):329-38.
2010-05-15 | E-GEOD-17363 | biostudies-arrayexpress
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis). We are working with an enzyme able to directly transfer sialyl residues among macromolecules known as the trans-sialidase. It constitutes a virulence factor from Trypanosoma cruzi, the agent of the Chagas' Disease the American trypanosomiasis. We described the ability of this virulence factor to induce thymocyte apoptosis in vivo that happens after silayl residue mobilization. The apoptosis is mediated by the thymic epithelial cells in the nurse cell complex. By employing the microarray approach we wish to analyze the gene expression induced in the thymus after TS treatment. Examination of differential expression in thymocytes between male and female mice of genes related to glycosylation. RNA samples (in triplicate) purified from thymocytes were analyzed by Glyco-gene Chip analysis.
2011-02-04 | E-GEOD-27054 | biostudies-arrayexpress
Project description:As Trypanosoma cruzi, the etiological agent of Chagas disease, multiplies in the cytoplasm of nucleated host cells, infection with this parasite is highly likely to affect host cells. We performed an exhaustive transcriptome analysis of T. cruzi-infected HeLa cells using an oligonucleotide microarray containing probes for greater than 47,000 human gene transcripts. In comparison with uninfected cells, those infected with T. cruzi showed greater than threefold up-regulation of 41 genes and greater than threefold down-regulation of 23 genes. Real-time reverse transcriptase-polymerase chain reaction (RT-PCR) of selected, differentially expressed genes confirmed the microarray data. Many of these up- and down-regulated genes were related to cellular proliferation, including seven up-regulated genes encoding proliferation inhibitors and three down-regulated genes encoding proliferation promoters, strongly suggesting that T. cruzi infection inhibits host cell proliferation, which may allow more time for T. cruzi to replicate and produce its intracellular nests. These findings provide new insight into the molecular mechanisms by which intracellular T. cruzi infection influences the host cell, leading to pathogenicity. Keywords: infection response
2008-02-06 | GSE7047 | GEO