Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global microRNA profiling of the mouse ventricles during development of severe hypertrophic cardiomyopathy and heart failure

ABSTRACT: The study sought to determine the global miRNA profile of ventricles during early and end-stage hypertrophic cardiomyopathy in a severe double mutant mouse model of the disease. MicroRNA expression profiles of ventricles of transgenic mice with a mutation in both the myosin heavy chain gene (MYH7 Arg403Gln) and cardiac troponin I gene (TNNI3 Ser203Gln) and of non-transgenic mice were determined using Rodent TaqMan Low Density miRNA Arrays A v2.0 (TLDA, Life Technologies). MicroRNA profiles were measured at 10 days of age and 16 days of age, in 3 biological replicates.

ORGANISM(S): Mus musculus

PROVIDER: GSE37692 | GEO | 2012/05/11

SECONDARY ACCESSION(S): PRJNA165683

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Global microRNA profiling of the mouse ventricles during development of severe hypertrophic cardiomyopathy and heart failure

Project description:The study sought to determine the global miRNA profile of ventricles during early and end-stage hypertrophic cardiomyopathy in a severe double mutant mouse model of the disease. MicroRNA expression profiles of ventricles of transgenic mice with a mutation in both the myosin heavy chain gene (MYH7 Arg403Gln) and cardiac troponin I gene (TNNI3 Ser203Gln) and of non-transgenic mice were determined using Rodent TaqMan Low Density miRNA Arrays A v2.0 (TLDA, Life Technologies). MicroRNA profiles were measured at 10 days of age and 16 days of age, in 3 biological replicates. qRT-PCR analysis of microRNAs of ventricles of three transgenic mice and three non-transgenic mice age 10 days, and three transgenic mice and three non-transgenic mice age 16 days. 450 ng RNA was reverse transcribed, without pre-amplification, using TaqMan MicroRNA Reverse Transcription Kit and Megaplex RT Primers rodent pool A (Life Technologies). Complementary DNA (cDNA) was amplified using a TaqMan rodent microRNA A Array v2.0 (Life Technologies) with TaqMan Universal PCR Master Mix on an ABI 7900HT Sequence Detection System.

2012-05-11 | E-GEOD-37692 | biostudies-arrayexpress

Activation of ERRγ enhances mitochondrial and sarcomere maturation in human induced pluripotent stem cell-derived cardiomyocytes

Project description:We identified two cardiac maturation stimulators from 9,048 compounds using Troponin I1 (TNNI1) and Troponin I3 (TNNI3) double reporter hiPSC-derived CMs. An estrogen-related receptor gamma (ERRγ)-specific agonist increased the size of hiPSC-CMs and their mitochondrial content and enhanced their mitochondrial function. In addition, combination of this agonist with an inhibitor of S-phase kinase-associated protein 2 (SKP2) increased the TNNI3 expression more highly than previous methods and enhanced cardiac maturation-related gene expression profiles.

2021-04-19 | GSE135319 | GEO

miRNA expression in primary human leukaemic B-cells from peripheral blood and after culture on stromal cells in the presence and absence of CD154 and IL-4

Project description:Dynamic miRNA expression data in 377 miRNA present on Taqman low density array (TLDA) Human MicroRNA Array (A) plates (Applied Biosystems, #4398965).

2011-11-03 | GSE24694 | GEO

Parallel genetic excisions of the cardiac troponin I N-terminal extension in tachycardic mammals

Project description:A study of cardiac troponin I evolution in mammals with high heart rates, including shrews, moles, and bats. With genomic, mRNA and protein level analyses we showed repeated loss of the N-terminal extension. Here, liquid chromatography with tandem mass spectrometry was used to verify cardiac troponin I (TNNI3) protein identity in ∼22 kDa bands from Pyrenean desman (Galemys pyrenaicus) and northern short-tailed shrew (Blarina brevicauda) hearts.

2024-07-19 | PXD048600 | Pride

Transcription profiling of mouse ventricles of IGF1R, IGF1R-caPI3K, IGF1R-dnPI3K, caPI3K, dnPI3K transgenic female mice at 3 months of age vs. non transgenic littermate controls

Project description:IGF1 and IGF1 receptors (IGF1R) are present in the adult heart and have been shown to be essential for myocardial performance. Insulin-like growth factor 1 (IGF1) is produced in numerous tissues particularly by the liver in response to growth hormone stimulation and is an important factor in the regulation of post-natal growth and development. We have generated and characterized transgenic mice over-expressing the IGF1R. We crossed IGF1R transgenic mice with dominant negative (dn)PI3K (p110) and with constitutively active (ca)PI3K(p110) transgenic mice. Expression profiling was performed on the ventricles of IGF1R, IGF1R-caPI3K, IGF1R-dnPI3K, caPI3K, dnPI3K transgenic female mice at 3 months of age. Non-transgenic littermates were used as controls.

2007-09-29 | E-GEOD-1143 | biostudies-arrayexpress

Genetic excision of the regulatory cardiac troponin I extension in high heart rate mammal clades

Project description:Mammalian cardiac troponin I (cTnI) contains a highly conserved N-terminal extension harboring protein kinase A targets (Ser23/24) which are phosphorylated during ß-adrenergic stimulation to increase cardiomyocyte relaxation rate. Here, we show that the Ser23/24 encoding exon 3 of TNNI3 was pseudoexonized multiple times in shrews and moles to mimic Ser23/24 phosphorylation without adrenergic stimulation, thereby facilitating the evolution of exceptionally high resting heart rates (~1000 beats min-1). We further reveal alternative splicing of TNNI3 exon 3 in distantly related bat families with both cTnI isoforms being incorporated into cardiac myofibrils.

2024-07-19 | PXD051845 | Pride

Proteomic profiling of a large cohort of HCM patients: genotype-specific protein changes

Project description:Hypertrophic cardiomyopathy (HCM) is characterized by asymmetric left ventricular (LV) hypertrophy and diastolic dysfunction, which leads to LV outflow tract obstruction (LVOTO) in the majority of cases. Mutations in genes encoding sarcomeric proteins cause HCM and are identified in more than half of the patients (sarcomere-mutation positive, SMP). Currently, more than 1500 HCM-causing mutations are known. Approximately 80% of mutations are located in the MYH7 and MYBPC3 genes, encoding for the thick filament proteins β-myosin heavy chain (β-MHC) and cardiac myosin-binding protein C (cMyBP-C), respectively. Less frequent are mutations in the TNNT2 and TNNI3 genes, encoding for the thin filament proteins cardiac troponin T (cTnT) and I (cTnI). Here, we applied an unbiased proteomics approach in a large number of myectomy samples from a clinically well-characterized HCM patient group to define HCM-specific derailments as well as genotype-specific changes at protein level. Our study shows that the downregulation of metabolic pathways and the upregulation of extracellular matrix proteins are the most prominent HCM-specific disease characteristics that are present in all samples independent of their genotype.

2021-01-14 | PXD012467 | Pride

Heart Failure Associated Changes in Alternative Splicing of Sarcomere Genes

Project description:Alternative mRNA splicing is an important mechanism for regulation of gene expression. Changes in gene expression contribute to the pathogenesis of heart failure. However, changes in mRNA splicing have not been systematically examined in heart disease. We hypothesized that mRNA splicing is changed in diseased hearts. We used the Affymetrix exon array, which separately measures expression of each known and computationally predicted exon, to globally evaluate changes in mRNA splicing in left ventricular myocardial RNA from control and ischemic cardiomyopathy (ICM) patients. We found that mRNA splicing is systematically changed in heart failure. RTPCR validated 9 previously unreported alternative splicing events. Furthermore, we demonstrated that the splicing of four key sarcomere genes, cardiac troponin T (TNNT2), cardiac troponin I (TNNI3), myosin heavy chain 7 (MYH7), and filamin C (FLNC), was significantly altered in ICM. Altered splicing of these genes in heart disease was confirmed in independent ICM samples, and in dilated cardiomyopathy and aortic stenosis. The minor variant fraction of these five genes was sufficient to classify samples into control or disease groups with 95% accuracy. Our data indicate that alternative splicing is systematically altered in human heart disease, suggesting that disease-associated perturbation of RNA splicing may contribute to the pathogenesis and development of heart failure. Disease-related changes in splicing of sarcomere genes may directly impact cardiomyocyte function.

2010-01-11 | GSE16499 | GEO

RNA-Seq Analyses of TGAC8 and WT mouse Left Ventricles

Project description:8 LV samples from WT and TGAC8 mouse hearts were analyzed. Mice were 3 m.o. Human ADCY8 gene was overexpressed in mouse heart under cardiac-specific MYH7 promoter

2022-12-23 | GSE205234 | GEO

Transcriptome profiling of left ventricles from cardiac-specific GRK-beta1AR transgenic and/or miR-150 transgenic mice treated with isoproterenol.

Project description:Genome-wide transcriptomic analyses in left ventricles (LVs) from cardiac-specific GRK-beta1AR transgenic (TG) and/or miR-150 TG mice treated with isoproterenol (ISO) were performed to identify novel targets of beta-arrestin-mediated beta1AR signaling and miR-150 in the heart.

2023-01-01 | GSE199195 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data