Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

In vivo BioID Mouse heart masspec data

ABSTRACT: Cardiac excitation-contraction (E-C) coupling requires dyads, the nanoscopic microdomains formed adjacent to Z-lines by apposition of transverse (T)-tubules and junctional sarcoplasmic reticulum (jSR). Disruption of dyad architecture and function are common features of diseased cardiomyocytes. However, little is known about the mechanisms that modulate dyad organization during cardiac homeostasis and disease. Here, we used proximity proteomics in intact, living hearts to identify proteins enriched near dyads.

INSTRUMENT(S): LTQ Orbitrap Velos, LTQ

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

SUBMITTER: Fujian Lu

LAB HEAD: William T. Pu

PROVIDER: PXD028960 | Pride | 2022-02-21

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Similar Datasets

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

Interplay between calcium cycling and sarcomeres directs cardiomyocyte redifferentiation and maturation during regeneration

Project description:Zebrafish hearts can regenerate by replacing damaged tissue with new cardiomyocytes. Although the steps leading up to the proliferation of surviving cardiomyocytes have been extensively studied, little is known about the mechanisms that control proliferation and redifferentiation to a mature state. We found that the cardiac dyad, a structure that regulates calcium handling and excitation-contraction coupling, played a key role in the redifferentiation process. A component of the cardiac dyad called leucine-rich repeat–containing 10 (Lrrc10) acted as a negative regulator of proliferation, prevented cardiomegaly, and induced redifferentiation. We found that its function was conserved in mammalian cardiomyocytes. This study highlights the importance of the underlying mechanisms required for heart regeneration and their application to the generation of fully functional cardiomyocytes.

2023-05-19 | GSE224156 | GEO

Gene expression profiling of wildtype vs. transgenic mice expressing the cardiac specific genetically encoded FRET biosensor Epac1-PLN

Project description:3’,5’-cyclic adenosine monophosphate (cAMP) is an ubiquitous second messenger which regulates multiple physiological functions by acting in distinct subcellular microdomains. Although several targeted cAMP biosensors have been developed and used in cell lines or neonatal cardiomyocytes, it is unclear whether such biosensors can be successfully used in vivo, especially in the context of disease. Here, we generated the first transgenic mouse model expressing a targeted cAMP sensor (Epac1-PLN) and analyzed microdomain-specific second messenger dynamics in the vicinity of the sarcoplasmic reticulum calcium ATPase (SERCA). We demonstrate the biocompatibility of this targeted sensor and its potential for real-time monitoring of compartmentalized cAMP signaling in adult cardiomyocytes isolated from healthy mouse heart and from in vivo cardiac disease model. Finally, we used gene arrays to verify that the mRNA expression levels of the main players involved in cAMP signaling such as beta-ARs, G-protein, adenylyl cyclases, PKAs, PDEs, and Epac were not significantly changed between wildtype and transgenic Epac1-PLN expressing cardiomyocytes. To compare cardiac specific mRNA expression between wildtype and Epac1-PLN transgenic mice, cardiomyocyte RNA from total of 5 individual wildtype and 5 Epac1-PLN transgenic mice was isolated and submitted for the Illumina gene array analysis to the Göttingen transcriptome analysis laboratory (TAL).

2015-03-02 | E-GEOD-65651 | biostudies-arrayexpress

Gene expression profiling of wildtype vs. transgenic mice expressing the cardiac specific genetically encoded FRET biosensor Epac1-PLN

2015-03-02 | GSE65651 | GEO

Transcriptional changes during Isoproterenol induced cardiac fibrosis in mice

Project description:Introduction: β-adrenergic stimulation using β-agonists such as isoproterenol has been routinely used to induce cardiac fibrosis in experimental in animal models. While transcriptome changes in surgical models of cardiac fibrosis such as Transverse aortic constriction (TAC), and coronary artery ligation (CAL) are well-studied, transcriptional changes during isoproterenol induced cardiac fibrosis is not well explored. Methods: Cardiac fibrosis was induced in male C57BL6 mice by administration of isoproterenol for 4, 8 or 11 days at 50mg/kg/day dose. Temporal changes in gene expression were studied by RNA sequencing. Results: We observed a significant alteration in the transcriptome profile across the different experimental groups compared to the saline group. Isoproterenol treatment caused upregulation of genes associated with ECM organization, cell-cell contact, three-dimensional structure, and cell growth, while genes associated with fatty acid oxidation, sarcoplasmic reticulum calcium ion transport, and cardiac muscle contraction are downregulated. A number of known long non-coding RNAs (lncRNAs) and putative novel lncRNAs exhibited differential regulation. Conclusion: In conclusion, our study shows that isoproterenol administration leads to the deregulation of genes relevant to ECM deposition and cardiac contraction and serves as an excellent alternate model to the surgical models of heart failure.

2023-11-02 | GSE239653 | GEO

Transcriptome analysis of mouse cardiac hypertrophy

Project description:RNA-Seq analysis of mouse cardiac transcriptome. Transverse aortic contraction was used to induce cardiac hypertrophy (TAC). To compare wild type and physiological cardiac hypertrophy 'Sendetary' (feeding mouse during 4 weeks) and 'Swim (exercise training to induce the cardiac hypertrophy) samples were analysed.

2012-05-11 | E-MTAB-727 | biostudies-arrayexpress

Cardiac Stretch-Induced Transcriptomic Changes are Axis-Dependent

Project description:The goal of this study was to examine the effect of the major axis of biaxial mechanical stretch on cardiac myocyte gene expression and to identify the signaling pathways and transcription factors regulating these changes. Neonatal cardiac myocytes were cultured on a micropatterned substrate, and the primary stretch axis was applied either parallel or transverse to the myofibril direction. RNA sequencing was conducted to study whole genomic expression changes after acute cardiac myocyte stretch. The results showed a more robust gene response to longitudinal than to transverse stretch. After 30 minutes of stretch, 53 and 168 genes were considered differentially expressed (DE) from transverse and longitudinal stretch, respectively. After 4 hours, the number of DE genes increased to 795 in longitudinal stretch while it decreased to 35 in transverse stretch. Gene ontology term (GO) analysis indicated enrichment of TF activity and protein kinase activity by both stretch axes; whereas longitudinal but not transverse stretch caused expression of genes involved in sarcomere organization and cytoskeletal protein binding.

2019-06-01 | GSE83655 | GEO

Loss of ADAM15 exacerbates transition to decompensated hypertrophy through activation of calcineurin pathway

Project description:Label-free quantification of cardiac tissue following transverse aortic constriction (TAC) in a WT and ADAM15-/- mouse model.

2022-03-07 | MSV000089016 | MassIVE

Differential gene expression in adrenal medulla after cardiac pressure overload

Project description:Transcriptom analysis of microdissect adrenal medulla after 8 weeks of cardiac pressure overload caused by transverse aortic constriction. Comparative transcriptome analysis was determined using the GeneChip Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA, USA). Six microarrays from microdissected adrenal medulla of mice were performed 8 weeks after transverse aortic constriction or sham operation.

2011-05-03 | E-GEOD-21829 | biostudies-arrayexpress

Differential gene expression in stellate sympathetic ganglia after cardiac pressure overload

Project description:Transcriptom analysis of stellate sympathetic ganglia after 8 weeks of cardiac pressure overload caused by transverse aortic constriction. Comparative transcriptome analysis was determined using the GeneChip Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA, USA). Six microarrays from stellate sympathetic ganglia of mice were performed 8 weeks after transverse aortic constriction or sham operation.

2010-02-25 | E-GEOD-18004 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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