Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

64 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mapping the cellular and molecular landscape of cardiac non-myocytes in murine type-2 diabetes

ABSTRACT: Here we define key single-cell transcriptional alterations within cardiac non-myocytes, from ventricles of spontaneously type-2 diabetic (db/db) and control (db/h) mouse hearts ([B6.BKS(D)-Lepr/J], stock #000697). The cell preparation sequenced consisted of metabolically active, live and nucleated non-myocyte cells, which were depleted of endothelial cells. The objective of this experiment was to develop a framework for understanding the dynamics of cardiac cell networks in murine type-2 diabetes, as a resource for future mechanistic studies.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Mus musculus

SUBMITTER: Malathi Dona

PROVIDER: E-MTAB-11940 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Analysis of the transcriptome of adult cardiac myocytes stimulated with CTGF

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. Primary, adult cardiac myocytes were cultured in the absence (n=6) or presence (n=6) of 200 nmol/L recombinant CTGF for 48 hours.

2015-02-01 | E-GEOD-36073 | biostudies-arrayexpress

Single cell RNA-Seq of the mouse heart in response to chronic stress

Project description:We characterized single-cell transcriptional profiles of heart ventricles of C57BL/6J female and male mice subjected to a chronic stress, two weeks of continuous administration of Angiotensin II. The cell preparation we sequenced consisted of metabolically active, nucleated non-myocyte cells which were depleted of endothelial cells, mixed with nuclei isolated from cardiomyocytes. The goal of this experiment included characterizing cellular diversity in stressed and unstressed hearts, uncovering potential drivers of cardiac fibrosis and hypertrophy, and quantifying sexual dimorphism in cardiac gene expression.

2020-11-24 | E-MTAB-8810 | biostudies-arrayexpress

RBFox2 regulates a broad RNA program and is required for genome-wide targeting of polycomb complex

Project description:Increasing evidence suggests that diverse RNA binding proteins interact with regulatory RNAs to regulate transcription. RBFox2 is a ubiquitous RNA binding protein with prevalent expression in stem cells, heart, and brain. Here, we report a systematic dissection of the RBFox2-regulated RNA program in the mouse heart, demonstrating its essential function for organizing the contractile apparatus and excitation-contraction (EC) coupling by modulating alternative splicing and microRNA activity. In this analysis, we unexpectedly encounter a major functional intersection between RBFox2 and Polycomb Complex 2 (PRC2), revealing a central requirement for RBFox2 to mediate genome-wide targeting of the PRC2 complex and transcriptional repression via chromatin-associated nascent RNAs. These findings unveil the mechanism underlying the enigmatic association of PRC2 with numerous active genes, highlight the importance of gene body sequences to gauge transcriptional output, and suggest nascent RNAs as critical signals for transcriptional feedback control to maintain homeostatic gene expression in mammalian cells. RASL-seq in cardiac myocytes (from WT and RBFox2 KO mouse hearts at ages of week 5, week 9 and week 18); RBFox2 whole cell and nucleus CLIP-seq in cardiac myocytes (from WT mouse hearts at age of week 9); Ago2 CLIP-seq in cardiac myocytes (from WT and RBFox2 KO mouse hearts at age of week 9); 3'-end RNA-seq in cardiac myocytes (from WT and RBFox2 KO mouse hearts at age of week 9); GRO-seq in mouse hearts (from WT and RBFox2 KO mice at age of week 9) and cultured MEF cells (negative control RNA, RBFox2 siRNA or SUZ12 siRNA treatment); RBFox2 and SUZ12 CHIP-seq in mouse hearts(from WT mice at age of week 9); RBFox2, SUZ12 and H3K27me3 CHIP-seq in cultured MEF cells (negative control RNA, RBFox2 siRNA or SUZ12 siRNA treatment, DRB treatment).

2015-10-22 | E-GEOD-57926 | biostudies-arrayexpress

Transcription profiling by array and functional characterization of developing cardiomyocytes from recombinant murine embryonic stem cells

Project description:Here, we characterize the transcriptome of the mouse embryonic stem cell line CM7-1 during differentiation into beating cardiomyocytes and compared the gene expression profiles with those from primary adult murine cardiomyocytes and left ventricular myocardium.

2009-03-21 | E-MEXP-1405 | biostudies-arrayexpress

Title Page Cardiac Gene Therapy Rescues Diabetic Cardiomyopathy and Lowers Blood Glucose

Project description:Diabetic cardiomyopathy, an increasingly global epidemic and a major cause of heart failure with preserved ejection fraction (HFpEF), is associated with hyperglycemia, insulin resistance, and intra-cardiomyocyte calcium mishandling. Here we identify that, in db/db mice with type 2 diabetes induced HFpEF, abnormal remodeling of cardiomyocyte transverse-tubule microdomains occurs with downregulation of the membrane scaffolding protein cardiac bridging integrator 1 (cBIN1). Transduction of cBIN1 by AAV9 gene therapy can restore transverse-tubule microdomains to normalize intracellular distribution of calcium handling proteins and, surprisingly, glucose transporter 4 (GLUT4). Cardiac proteomics revealed that AAV9-cBIN1 normalizes components of calcium handling and GLUT4 translocation machineries. Functional studies further identified that AAV9-cBIN1 normalizes insulin-dependent glucose uptake in diabetic cardiomyocytes. Phenotypically, AAV9-cBIN1 rescues cardiac lusitropy, improves exercise intolerance, and ameliorates hyperglycemia in diabetic mice. Restoration of transverse-tubule microdomains can improve cardiac function in the setting of diabetic cardiomyopathy, and also improve systemic glycemic control.

2023-10-24 | PXD044236 | Pride

RNA-Seq of Kidney Glomeruli from Type 2 diabetic (db/db) and non-diabetic mice

Project description:We investigated the gene expression profiles of RNA isolated from kidney glomeruli from aged, 25 week old type-2 diabetic (db/db) and non-diabetic mice. In order to investigate the consequences of hyperglycemia on the pathogenesis and progression of diabetic nephropathy Kidney glomeruli from 3 diabetic and 3 non-diabetic, control mice were isolated and RNA purified for RNA-Seq analysis on the Illumina HiSeq 2000. The goal of the project was to generate comprehensive list of noncoding RNA genes differentially regulated between the two conditions in order to identify novel targets for further study.

2016-10-24 | E-GEOD-77717 | biostudies-arrayexpress

Influenza virus infection leads to global cardiac proteome remodeling during convalescence

Project description:Influenza virus infection leads to global cardiac proteome remodeling during convalescence MTD project_description "Influenza virus infections lead to more than 500,000 hospitalizations in the U.S. every year. Patients with cardiovascular diseases have been shown to be at high risk of influenza mediated cardiac complications. Importantly, recent reports have provided clinical data supporting a direct link between laboratory-confirmed influenza virus infection and adverse cardiac events. However, the molecular mechanisms of how influenza virus infection induces detrimental cardiac changes, even after resolution of the pulmonary infection, is completely unknown.

2022-04-01 | PXD015992 | Pride

Transcriptional profiling by array to study the effect of adenoviruses encoding the FLAG epitope or full-length antisense sequence to Atf3 on transcriptional regulation in rat cardiac myocytes

Project description:Cardiomyocytes, the terminally-differentiated contractile cells of the heart, undergo hypertrophic growth in response to endothelin-1. This is associated with changes in mRNA expression of immediate early genes (IEGs). Atf3 is a member of the ATF/CREB family transcription factors which bind as dimers to the cAMP response element (CRE). Atf3 mRNA is particularly associated with cell stress responses and is implicated in negative feedback regulation of gene expression. We confirmed that endothelin-1 promotes expression of Atf3 mRNA and protein in cardiomyocytes and that it is an IEG. Atf3 expression was transient and maximal at 0.5-1 h. We used adenoviruses for expression of antisense Atf3 RNA in cardiomyocytes to inhibit upregulation of Atf3 protein in response to endothelin-1. The effects on the cardiomyocyte transcriptome in control cells and cells exposed to endothelin-1 were examined using Affymetrix rat exon 1.0 ST arrays with data analysis using GeneSpring GX11.5. We identified transcripts that were upregulated by endothelin-1 for which antisense Atf3 significantly (FDR<0.05) enhanced or inhibited expression, respectively. The basal levels of other transcripts that are upregulated by endothelin-1 were also increased by antisense Atf3, though antisense Atf3 had no further effect on the response to endothelin-1. The data were validated by quantitative PCR of selected IEG mRNAs examining the effects at different times.

2012-10-01 | E-MEXP-3392 | biostudies-arrayexpress

Profiling pancreatic islets from obese db/db and lean control db/+ mice

Project description:This program addresses the molecular basis of beta-cell failure associated with the development of type 2 diabetes in the db/db mice. Specifically, which genes are differentially expressed in pancreatic islets of the db/db mice compared to the control db/+ mice? The db/db mice islets profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the islets of db/db mice compared to the corresponding db/+ controls.

2013-03-22 | E-GEOD-31953 | biostudies-arrayexpress

Profiling epididymal white adipose tissue (eWAT) from obese db/db and lean control db/+ mice

Project description:This program addresses the gene signature associated with the development of type 2 diabetes in the db/db mice. Specifically, which genes are differentially expressed in adipose tissue of the db/db mice compared to the control db/+ mice? The db/db mice eWAT profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the eWAT of db/db mice compared to the corresponding db/+ controls.

2013-03-22 | E-GEOD-38082 | biostudies-arrayexpress

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