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SRP101375
Mus musculus
4 Downloadable Samples
Illumina HiSeq 2500
Description
Control and H3K9me3-depleted (KDM4D OE) adult cardiac myocytes
Publication Title
No associated publication
Sample Metadata Fields
Sex, Age, Specimen part, Cell line
View Samples SRP059989- Homo sapiens
- 10 Downloadable Samples
- IlluminaHiSeq2000
Description
By means of 3' end sequencing we provide a genome-wide, high-resolution polyadenylation map of the human heart. By sequencing 5 control en 5 dilated cardiomyopathy (DCM) myocardial specimens we investigate the difference in alternative polyadenylation (APA) in healthy and diseased hearts.
Publication Title
Genome-Wide Polyadenylation Maps Reveal Dynamic mRNA 3'-End Formation in the Failing Human Heart.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Class IIa histone deacetylases (HDACs) are signal-responsive regulators of gene expression involved in vascular homeostasis. To investigate the differential role of class IIa HDACs for the regulation of angiogenesis, we used siRNA to specifically suppress the individual HDAC isoenzymes. Among the HDAC isoforms tested, silencing of HDAC5 exhibited a unique pro-angiogenic effect evidenced by increased endothelial cell migration, sprouting and tube formation. Consistently, overexpression of HDAC5 decreased sprout formation, indicating that HDAC5 is a negative regulator of angiogenesis. The anti-angiogenic activity of HDAC5 was independent of MEF2 binding and its deacetylase activity, but required a nuclear localization indicating that HDAC5 might affect the transcriptional regulation of gene expression. To identify putative HDAC5 targets, we performed microarray expression analysis. Silencing of HDAC5 increased the expression of fibroblast growth factor 2 (FGF2) and angiogenic guidance factors including Slit2. Antagonization of FGF2 or Slit2 reduced sprout induction in response to HDAC5 siRNA. ChIP assays demonstrate that HDAC5 binds to the promoter of FGF2 and Slit2. In summary, HDAC5 represses angiogenic genes, like FGF2 and Slit2, which causally contribute to capillary-like sprouting of endothelial cells. The de-repression of angiogenic genes by HDAC5 inactivation may provide a useful therapeutic target for induction of angiogenesis.
Publication Title
HDAC5 is a repressor of angiogenesis and determines the angiogenic gene expression pattern of endothelial cells.
Sample Metadata Fields
Specimen part
View Samples- Rattus norvegicus
- 6 Downloadable Samples
- Illumina HiSeq 3000
Description
In the present study, we used NGS to characterise lncRNA-seq of acute myocardial infarction (AMI) rats and healthy controls to elucidate the functions and mechanisms of lncRNAs in cardiomyocytes. We want to identified a certain pair of lncRNA and its binding mRNA to elucidate the role in ischemia-hypoxia cardiomyocytes for AMI.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part, Cell line, Treatment
View Samples- Danio rerio
- 4 Downloadable Samples
- Illumina HiSeq 2500
Description
to study the feasibility of gene therapy of TNNT2 mutant related cardiomyopathy
Publication Title
No associated publication
Sample Metadata Fields
Sex, Age, Specimen part, Cell line
View Samples- Homo sapiens
- 18 Downloadable Samples
- Illumina HiSeq 3000
Description
Aims: Cardiovascular disease, one of the most common causes of death in western populations, is characterized by changes in RNA splicing and expression. Circular RNAs (circRNA) originate from back-splicing events, which link a downstream 5’ splice site to an upstream 3’ splice site. Several back-splicing junctions (BSJ) have been described in heart biopsies from human, rat and mouse hearts.[1,2] Here, we use human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs) to identify circRNA and host gene dynamics in cardiac development and disease. In parallel, we explore candidate interactions of selected homologs in mouse and rat via RIP-seq experiments.Methods and Results: Deep RNA sequencing of cardiomyocyte development and ß-adrenergic stimulation uncovered 4,518 circRNAs. The set of circular RNA host genes is enriched for chromatin modifiers and GTPase activity regulators. RNA-seq and qRT-PCR data showed that circular RNA expression is highly dynamic in the hiPSC-CM model with 320 circRNAs showing significant expression changes. Intri-guingly, 82 circRNAs are independently regulated to their host genes. We validated the same circRNA dynamics for circRNAs from ATXN10, CHD7, DNAJC6 and SLC8A1 in biopsy material from human dilated cardiomyopathy (DCM) and control patients. Finally, we could show that rodent homologs of circMYOD, circSLC8A1, circATXN7 and circPHF21A interact with either the ribosome or Argonaute2 protein complexes.Conclusion: CircRNAs are dynamically expressed in a hiPSC-CM model of cardiac development and stress response. Some circRNAs show similar, host-gene inde-pendent expression dynamics in patient samples and may interact with the ribo-some and RISC complex. In summary, the hiPSC-CM model uncovered a new sig-nature of potentially disease relevant circRNAs which may serve as novel therapeu-tic targets.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part, Race
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
Myocardial infarction (MI) is one of the most severe manifestations of coronary artery disease (CAD) and the leading cause of death from non-infectious diseases worldwide. It is known, that the central component of CAD pathogenesis is a chronic vascular inflammation. However, the mechanisms underlying the changes that occur in T, B and NK-lymphocytes, monocytes and other immune cells during CAD and MI are still poorly understood. One of those pathogenic mechanisms might be the dysregulation of intracellular signaling pathways in the immune cells.
Publication Title
Collapsing the list of myocardial infarction-related differentially expressed genes into a diagnostic signature.
Sample Metadata Fields
Sex, Specimen part, Disease stage
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The genetics, social, cultural and environmental factors pose a great challenge for the diagnosis and treatment of coronary heart disease among different racial groups. We aimed to identify the differentially expressed genes involved in coronary heart disease in Chinese Han people as an aid for screening and diagnosing coronary heart disease.
Publication Title
No associated publication
Sample Metadata Fields
Age, Specimen part, Disease, Disease stage, Race
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The genes had different expression between healthy people and acute myocardial infarction.We aimed to identify the differentially expressed genes involved in acute myocardial infarction in Northeast Chinese Han people.
Publication Title
No associated publication
Sample Metadata Fields
Age, Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 24 Downloadable Samples
- Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)
Description
ASCs cultured in complete medium, ASCs cultured in serum serum-deprived medium, and ASCs stimulated with VEGF in serum-deprived medium were compared. Using microarray analysis, gene expression from the whole genome was compared between conditions. Compared to ASCs in complete medium, expression of 190 and 108 ASC genes were significantly regulated altered by serum deprivation and serum deprivation combined with VEGF, respectively. No significant differences in gene expression patterns between serum-deprived ASCs and serum-deprived ASC combined with VEGF stimulation were found. Genes most prominently and significantly up-regulated by both conditions were growth factors (IGF1, BMP6, PDGFD, FGF9), adhesion molecule CLSTN2, extracellular matrix related proteins like matricellular proteins SMOC2, SPON1 and ADAMTS12, and inhibitors of proliferation (JAG1). The most significantly down-regulated genes included matrix metalloproteinases (MMP3, MMP1), and proliferation markers (CDKN3) and GREM2, - a BMP6 antagonist.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part, Subject
View Samples