Transcriptional Remodeling in Human Cardiac Fibroblasts and Myocytes Induced by Oxygen-Dependent Crosstalk
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PROVIDER: PRJNA1072710 | ENA |
REPOSITORIES: ENA
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Project description:Myocardial infarctions are caused by coronary occlusions that deprive downstream myocardial tissue of oxygenated blood, leading to localized necrosis of cardiac myocytes. Hypoxic injury drives a remodeling process in which cardiac fibroblasts activate and synthesize matrix proteins to form a scar. During this process, cardiac cells are exposed to an oxygen gradient at the infarct border zone that transitions from 0% oxygen at the site of injury to 10% oxygen in healthy myocardium. However, the impact of any crosstalk between hypoxic cardiac fibroblasts and neighboring, normoxic (10% oxygen) cardiac cells is unexplored because conventional research tools cannot re-create spatially heterogeneous oxygen landscapes. Here, we used a microfluidic device to co-culture hypoxic cardiac fibroblasts with (1) normoxic cardiac fibroblasts or (2) normoxic human induced pluripotent stem cell (hiPSC)-derived cardiac myocytes. We then compared their transcriptome to the same cells cultured in uniform hypoxia or normoxia. These data contribute to more advanced understanding of how oxygen-dependent crosstalk between cardiac cells impacts the wound healing process post-myocardial infarction.
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2011-11-08 | E-MIMR-12 | biostudies-arrayexpress
Project description:siRNA knockdown of neonatal rat cardiac myocytes and fibroblasts
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Project description:Ischemic cardiomyopathy (ICM) leads to congestive heart failure and can cause sudden cardiac death due to arrhythmia. Existing molecular knowledge base of ICM is rudimentary because of lack of specific attribution to cell type and function. This study was designed to investigate cell-specific molecular remodeling of ion channels, exchangers and pumps, which are signaling molecules (SM) involved in electrical, signaling and mechanical functions of the heart. Atrial and ventricular myocytes were isolated by laser-capture microdissection from left atrium and ventricle of healthy and ICM human hearts. SM and their splice variants altered by ICM in cardiomyocytes were identified by splice microarray and validated by RT-PCR. Molecular profiling of ICM-related changes showed that SM in atrial and ventricular myocytes remodel following their unique programs. ICM affected 63 genes in ventricular myocytes and 12 genes in atrial myocytes. Only few of the identified genes were previously linked to human cardiac disfunctions. In our experiments we used 3 healthy hearts rejected from transplantation procedure and explanted ICM hearts from three male patients. Tissue samples were dissected from left ventricle and left atrial appendages. Atrial and ventricular myocytes were laser-capture microdissected from serial 7-8-µm thick cryostat sections. Individual cellular total RNA samples were analyzed on custom-built Human Ion Channel Splice Arrays slides (ExonHit) manufactured on the Ion Channel Splice Array sv1.1 platform representing 287 human SM, including 248 alternatively spliced ones in total 1655 splicing events and supplemented with capabilities to recognize connexins and ryanodine receptors.
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Project description:We report gene expression by RNAtag-seq after treatment with 75 different small molecule perturbations in culture of human iPSC-derived cardiac myocytes and genetically matched primary dermal fibroblasts. Perturbations were chosen from the SelleckChem Bioactive Library, among all molecules targeting any kinases or G-protein coupled receptors, and chosen to have as little overlap in annotated targets as possible. Based on these experiments (and others) we show that transcription factors important for cardiac development and cardiac myocyte identity maintenance were frequently up-regulated (i.e., "responsive") after small molecule perturbations of cultured iPSC-derived cardiac myocytes (i.e., responsive). We also show that the set of highly responsive transcription factors in fibroblasts are enriched for barriers to fibroblast reprogramming to iPSC.
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Project description:Ischemic cardiomyopathy (ICM) leads to congestive heart failure and can cause sudden cardiac death due to arrhythmia. Existing molecular knowledge base of ICM is rudimentary because of lack of specific attribution to cell type and function. This study was designed to investigate cell-specific molecular remodeling of ion channels, exchangers and pumps, which are signaling molecules (SM) involved in electrical, signaling and mechanical functions of the heart. Atrial and ventricular myocytes were isolated by laser-capture microdissection from left atrium and ventricle of healthy and ICM human hearts. SM and their splice variants altered by ICM in cardiomyocytes were identified by splice microarray and validated by RT-PCR. Molecular profiling of ICM-related changes showed that SM in atrial and ventricular myocytes remodel following their unique programs. ICM affected 63 genes in ventricular myocytes and 12 genes in atrial myocytes. Only few of the identified genes were previously linked to human cardiac disfunctions.
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Project description:Primary neonatal rat cardiac myocytes were isolated and subjected to siRNA mediated Yap knockdown
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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. 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: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