Single cell gene expression profiling of cardiac non-myocytes from CD31 depleted suspensions
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE200067 | GEO | 2022/04/06
REPOSITORIES: GEO
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Project description:Single cell gene expression profiling of cardiac non-myocytes from CD31 depleted suspensions
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2015-02-01 | E-GEOD-36073 | biostudies-arrayexpress
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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.
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Project description:Primary neonatal rat cardiac myocytes or fibroblasts were isolated and subjected to siRNA mediated Yap knockdown
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Project description:Transgenic mice with cardiac-restricted overexpression of connective tissue growth factor (CTGF) have substantially increased tolerance towards ischemia/reperfusion injury. In the transgenic mouse model, we found that CTGF induces expression of severeal genes putatively involved in cardioprotection. The purpose of this study was to determine gene expression in cardiac myocytes stimulated with purified, recombinant CTGF, comparing unstimulated and stimulated samples. The cytoprotective actions of CTGF was recflected in the transcriptome of CTGF-stimulated cardiac myocytes. Gene ontology analysis revealed that genes included under the terms anti-apoptosis, response to wounding, and response to stress were significantly overrepresented in cardiac myocytes exposed to CTGF. Serveral of the most higly up-regulated genes have previously been reported to exert cardioprotective actions and increase tolerance towards ischemia/reperfusion injury.
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