Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analysis of cardiac ischemia-reperfusion injury using DIA proteomics and N-terminomics

ABSTRACT: Data used in the publication: Analysis of cardiac ischemia-reperfusion injury using DIA proteomics and N-terminomics reveals alterations in mitochondrial function and metabolism

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Rattus (ncbitaxon:10114)

SUBMITTER: Olivier Julien

PROVIDER: MSV000092906 | MassIVE |

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Publications

Data-Independent Acquisition Proteomics and N-Terminomics Methods Reveal Alterations in Mitochondrial Function and Metabolism in Ischemic-Reperfused Hearts.

Hartley Bridgette B Bassiouni Wesam W Roczkowsky Andrej A Fahlman Richard R Schulz Richard R Julien Olivier O

Journal of proteome research 20240124 2

Myocardial ischemia-reperfusion (IR) (stunning) injury triggers changes in the proteome and degradome of the heart. Here, we utilize quantitative proteomics and comprehensive degradomics to investigate the molecular mechanisms of IR injury in isolated rat hearts. The control group underwent aerobic perfusion, while the IR injury group underwent 20 min of ischemia and 30 min of reperfusion to induce a stunning injury. As MMP-2 activation has been shown to contribute to myocardial injury, hearts a ...[more]

PMID: 38264990

Similar Datasets

Decorin protects cardiac myocytes against simulated ischemia/reperfusion injury

Project description:Primary cardiac myocytes isolated from neonatal Wistar rats were cultured and simulated ischemia/reperfusion injury were conducted on them in the presence or absence of decorin. Decorin is a small leucin-rich proteoglycan, which has a cardiocytoprotective effect. The underlaying mechanism of this cardiocytoprotective phenomenon is unknown, therefore our aim was to investigate the changes in the mRNA expression between the decorin (3nM) treated and vehicle-treated control cells.

2020-12-31 | E-MTAB-9325 | biostudies-arrayexpress

RNA-seq analysis of young swine following cardiac ischemia/reperfusion injury.

Project description:This study was a part of a larger study assessing the response of young pigs to cardiac ischemia/reperfusion (IR) injury. A mild cardiac injury approach (IR) was used in post-weaned pigs (1-month), to assess regenerative repair in young large mammals after transient ischemic injury. Female and male postnatal day (P)30 pigs were subjected to cardiac ischemia (1-hour) by occlusion of the left anterior descending artery followed by reperfusion (IR), or to sham operation. In pigs subjected to IR, myocardial damage occurred, indicated by increased circulating cardiac troponin I 2-hours post-ischemia. In addition, cardiac ejection fraction (EF) was significantly decreased 2-hours post-ischemia and reduced EF was maintained to the 4-week study end-point. Histology demonstrated evidence of CM cell cycling at 2-months of age in multinucleated CMs in both sham-operated and IR pigs. Following IR, regional scar formation and inflammation in the epicardial region proximal to injury were observed 4-weeks post-IR. Sex differences in cardiac function and collagen deposition were found, highlighting the importance of representing both sexes in cardiac injury studies. Together, our results describe an effective novel cardiac injury model in 1-month old swine, at a time when CM are still cycling. However, pigs subjected to IR show a prolonged decrease in cardiac function, and the formation of a small, regional scar with increased inflammation. Together, these data demonstrate that 1-month old pigs do not regenerate myocardium, but form a scar, after transient IR injury.

2020-04-27 | GSE137293 | GEO

Decorin protects cardiac myocytes against simulated ischemia/reperfusion injury

Project description:Decorin protects cardiac myocytes against simulated ischemia/reperfusion injury

| PRJEB39277 | ENA

Differential expression of cardiac mRNAs induced by Dexmedetomidine pretreatment in myocardial ischemia/reperfusion injury of mice

Project description:To investigate the cardioprotection of Dexmedetomidine, we established myocardial ischemia/reperfusion models in mice with vehicle or Dexmedetomidine pretreatment. We then performed mRNA sequencing of cardiac tissues and conducted gene expression profiling analysis.

2023-02-01 | GSE210873 | GEO

RealTime quantitative PCR of cardiac at risk area samples obtained from a mouse model of ischemia and reperfusion injury

Project description:Mice were exposed to cardiac ischemia/reperfusion injury and sacrificed after 1 or 4 days. Hearts were stained with Evans blu/TTC to isolate the at risk area. Hearts were divided into 1mm slices, the at risk area of any slice were pooled together before RNA extraction. Mice were divided into 3 different groups: Sham animals have been subjected to the surgical procedure without the induction of the ischemia and reperfusion injury and represent the control animals; LAD group is represented by animals subjected to the surgical procedure and the induction of the ischemia and reperfusion imjury; MLAD group is represented by animals subjected to the surgical procedure and the induction of the ischemia and reperfusion injury, followed by myriocin treatment (SLN/Myr) at the beginning of reperfusion.

2019-07-07 | GSE133913 | GEO

Proteomics analysis of cardiac tissues after ischemia reperfusion injury

Project description:In order to analysis the differentially expressed proteins after cardiac ischemia reperfusion injury, mice were either subjected into sham operation or left anterior descending of coronary artery ligation for 1 h, followed by 24 h reperfusion. Hearts were collected and proteomics analysis were carried out.

2023-02-15 | PXD040135 | iProX

Expression of Ciona intestinalis alternative oxidase (AOX) in a mouse model of cardiac ischemia-reperfusion

Project description:The objective of this study was to test how restoration of mitochondrial respiration using AOX affects the development of cardiac ischemia-reperfusion (IR) injuries in C57BL/ 6J mice. AOX transgenic mice have Ciona intestinalis AOX coding sequence knocked into the Rosa26 locus with AOX expression controlled by a CAG promoter as described elsewhere (Szibor et al. (2017) Dis Model Mech 10: 163–171). Consequences of 45 min of cardiac ischemia were studied 3 and 9 weeks after reperfusion in both wild-type and AOX litter mates.

2020-01-30 | PXD014061 | Pride

Proteomics analysis of cardiac extracellular matrix remodeling in a porcine model of ischemia/reperfusion injury: Infarcted, Guanidine

Project description:The aim of the present study is to characterize ECM remodeling after myocardial infarction by applying a proteomics method based on ECM enrichment and MS analysis to a porcine model of ischemia/reperfusion injury. The human-like physiology and anatomy of pigs facilitate comparisons of different cardiac regions to establish an accurate temporal and spatial pattern of the ECM remodeling process.

2016-04-07 | PXD003919 | Pride

Proteomics analysis of cardiac extracellular matrix remodeling in a porcine model of ischemia/reperfusion injury: control, guanidine

2016-04-07 | PXD003918 | Pride

Irisin deficiency exacerbates diet-induced insulin resistance and cardiac dysfunction and promotes ischemia and reperfusion injury

Project description:The myokine irisin is involved in the regulation of a variety of physiological conditions, metabolism, and survival. We and others have demonstrated that recombinant irisin contributes critically to modulation of insulin resistance and cardiac function. However, the molecular mechanisms by which irisin exerts its physiological effects on cardiac function and insulin sensitivity remain unclear. We utilized the CRISPR/Cas9 genome editing system to delete irisin. Irisin deficiency did not result in abnormalities in development, growth, or cardiac function; however, gene expression profiling showed that several key signaling pathways related to growth, insulin signaling, and integrin signaling were coordinately downregulated. However, loss of irisin resulted in more severe insulin resistance and metabolic derangement when mice were exposed to a high fat diet, which was associated with profound cardiac dysfunction and hypertrophic remodeling. In addition, the loss of irisin also exacerbated myocardial ischemia-reperfusion injury, as indicated by a reduction of post-ischemic ventricular function and an increase in infarct size. Taken together, our results indicate that loss of irisin exacerbates insulin resistance and cardiac depression in response to high fat diet and promotes myocardial ischemia-reperfusion injury. This evidence suggests a role for irisin in modulating insulin resistance, cardiac function and ischemic injury.

2023-11-08 | GSE231597 | GEO

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