E-PROT-62
Ontology highlight
ABSTRACT:
PROVIDER: E-PROT-62 | ExpressionAtlas | 2022-01-10
REPOSITORIES: ExpressionAtlas
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Project description:Genetic and genomic research has greatly advanced our understanding of heart disease; yet a comprehensive map of the protein landscape of living human hearts is still lacking. Here we set out to identify the molecular basis of functional differences between human cardiac chambers by comprehensive protein expression quantification from samples collected in vivo by high-resolution mass spectrometry. Cardiac biopsies of right atria (RA), left atria (LA) and left ventricle (LV) were obtained from seven humans undergoing open chest surgery and analyzed by high-resolution mass spectrometry. We identify hundreds of proteins with a chamber specific expression pattern, supporting the different functional roles of the cardiac chambers, enabling identification of chamber specific drug targets, and offering novel links between genomic data and the mechanisms of disease.
2020-06-15 | PXD008722 | Pride
Project description:Myocardial tissue samples were explanted from the explanted left ventricle of heart failure patients with DCM (n=4), left ventricular infarct, peri-, and non-infarct regions of HF patients with ICM (n=4) at the time of their heart transplant surgeries, and the left ventricle of age- and sex-matched non-failing controls (NFC, n=4). Comparative quantitative analysis was performed on three independent sets (DCM vs. NFC, infarct vs. non-infarct, and peri- vs. non-infarct) labeled with 10-plex tandem mass tags. Following enrichment of phosphorylated peptides, the flow-through and eluted fractions were collected separately and subjected to LC-MS/MS (liquid chromatography-tandem mass spectrometry) on a Q-Exactive HF for global proteomics and phosphoproteomics profiling respectively.
2023-11-20 | PXD012664 | Pride
Project description:Quantitative in vivo analyses reveal a complex pharmacogenomic landscape in lung adenocarcinoma
| PRJNA610595 | ENA
Project description:Mammalian heart development is built on highly conserved molecular mechanisms with polygenetic perturbations resulting in a spectrum of congenital heart diseases (CHD). However, the transcriptional landscape of cardiogenic ontogeny that regulates proper cardiogenesis remains largely based on candidate-gene approaches. Herein, we designed a time-course transcriptome analysis to investigate the genome-wide expression profile of innate murine cardiogenesis ranging from embryonic stem cells to adult cardiac structures. This comprehensive analysis generated temporal and spatial expression profiles, prioritized stage-specific gene functions, and mapped the dynamic transcriptome of cardiogenesis to curated pathways. Reconciling the bioinformatics of the congenital heart disease interactome, we deconstructed disease-centric regulatory networks encoded within this cardiogenic atlas to reveal stage-specific developmental disturbances clustered on epithelial-to-mesenchymal transition (EMT), BMP regulation, NF-AT signaling, TGFb-dependent induction, and Notch signaling. Therefore, this cardiogenic transcriptional landscape defines the time-dependent expression of cardiac ontogeny and prioritizes regulatory networks at the interface between health and disease. To interrogate the temporal and spatial expression profiles across the entire genome during mammalian heart development, we designed a time-course microarray experiment using the mouse model at defined stages of cardiogenesis, starting with embryonic stem cells (ESC, R1 stem cell line), early embryonic developmental stages: E7.5 whole embryos, E8.5 heart tubes, left and right ventricle tissues at E9.5, E12.5, E14.5, E18.5 to 3 days after birth (D3) and adult heart (Figure 1A). At each time point, microarray experiments were performed on triplicate biological samples. Starting at E9.5, tissue samples from left ventricles (LV) and right ventricles (RV) were microdissected for RNA purification and microarray analysis to determine spatially differential gene expression between LV and RV during heart development.
2014-05-19 | E-GEOD-51483 | biostudies-arrayexpress
Project description:The study performed NGS to investigate the cardiac transcriptomes of right and left ventricular heart specimens of 3-4-month-old BBLN-transgenic mice with FVB/N background in comparison to those of non-transgenic FVB/N mice. BBLN-transgenic (Tg-BBLN) mice with myocardium-specific BBLN expression were generated to investigate the cardiac phenotype of increased cardiac BBLN transcript levels because the function of BBLN (Bublin coiled-coil protein), which is the chromosome 9 open reading frame(C9orf16), is largely unknown. Tg-BBLN mice with increased cardiac BBLN levels developed features of heart failure with increasing age. Pathomechanisms of heart failure induced by BBLN were investigated by NGS of right and left ventricular heart specimens of male, BBLN-transgenic mice (age: 3-4 months). NGS data reveal transcriptome changes in right and left ventricular heart specimens induced by increased expression of BBLN in the heart.
2023-09-18 | GSE241022 | GEO
Project description:The RNA-binding protein RBM20 has been implicated in dilated cardiomyopathy (DCM), a major cause of chronic heart failure. To determine how RBM20 regulates alternative splicing, we combined transcriptome-wide CLIP-seq, RNA-seq, and quantitative proteomics in cell culture, rat, and human hearts. Our analyses revealed a distinct RBM20 RNA-recognition element in predominantly intronic binding sites and linked repression of exon splicing with RBM20-binding near 3prime- and 5prime-splice sites. Our proteomic data show RBM20 interaction with U1- and U2-snRNPs and suggests splicing repression through spliceosome stalling at complex A. Among direct RBM20 targets are several genes involved in DCM as well as new genes not previously associated with the disease process. In human failing hearts, we demonstrate that reduced expression levels of RBM20 affect alternative splicing of several direct targets, indicating that differences in RBM20 gene expression may affect cardiac function. These findings reveal a new mechanism to understand the pathogenesis of human heart failure. The provided data files for RNA-seq contain information for reads that map to human RBM20 only.
2014-11-11 | E-MTAB-2572 | biostudies-arrayexpress
Project description:Rats underwent surgery for LAD ligation for 30 min followed by reperfusion. Heart ventricles were collected 2d or 7d after reperfusion. Keywords: rat heart ventricles, LAD - left anterior descending coronary artery, IR - ischemia-reperfusion
2006-03-24 | GSE4105 | GEO
Project description:Pulmonary hypertension worsens outcome in left heart disease. Stiffening of the pulmonary artery may drive this pathology by increasing right ventricular dysfunction and lung vascular remodeling. We showed that pulmonary arteries from patients with left heart disease are characterized by increased stiffness that correlates with impaired pulmonary hemodynamics. Pulmonary arteries in left heart disease patients with pulmonary hypertension were characterized by degradation of elastic fibers paralleled by an accumulation of fibrillar collagens. We utilized RNA sequencing to identify differentially expressed genes regulating extracellular matrix remodeling in pulmonary arteries of left heart disease patients with or without pulmonary hypertension, in comparison to healthy-heart donor controls. As such we identified that transcriptional deregulation of extracellular matrix constituents and their regulators precedes clinical pulmonary hypertension, and therefore might be a pathomechanism that drives pulmonary arterial remodeling and stiffening in left heart disease.
2023-07-03 | GSE236251 | GEO
Project description:Cardiopoietic stem cells are in advanced clinical testing for ischemic heart failure. To profile their uncharted molecular influence on recipient hearts, systems proteomics was applied in a chronic murine model of infarction randomized with and without human cardiopoietic stem cell treatment. Four biological replicates are included from each of three separate groups, Control (Ctrl, n=4), myocardial infarction without treatment (MI, n=4), and MI with cardiopoietic stem cell treatment (CP, n=4). Athymic nude male mice (2-3 months of age) underwent left anterior descending coronary artery ligation (70-min occlusion followed by reperfusion). ST elevation on the electrocardiogram confirmed MI. Four weeks post-MI, animals were randomized into cohorts without (MI, n=4) or with (CP, n=4) cell therapy. Human CP cells were generated from bone marrow derived mesenchymal stem cells using an established cardiopoiesis protocol. Media (15 µL), with or without CP cells (600,000 cells/heart), were epicardially delivered in infarcted left ventricles.
2020-03-23 | PXD017381 | Pride
Project description:Left ventricular mass (LVM) and cardiac gene expression are complex traits regulated by factors both intrinsic and extrinsic to the heart. To dissect the major determinants of LVM, we combined expression quantitative trait locus1 and quantitative trait transcript (QTT) analyses of the cardiac transcriptome in the rat. Using these methods and in vitro functional assays, we identified osteoglycin (Ogn) as a major candidate regulator of rat LVM, with increased Ogn protein expression associated with elevated LVM. We also applied genome-wide QTT analysis to the human heart and observed that, out of 22,000 transcripts, OGN transcript abundance had the highest correlation with LVM. We further confirmed a role for Ogn in the in vivo regulation of LVM in Ogn knockout mice. Taken together, these data implicate Ogn as a key regulator of LVM in rats, mice and humans, and suggest that Ogn modifies the hypertrophic response to extrinsic factors such as hypertension and aortic stenosis. Experiment Overall Design: 7 cardiac biopsies from control patients and 20 cardiac biopsies from aortic stenosis patients
2008-11-15 | E-GEOD-10161 | biostudies-arrayexpress