Analysis of early changes in mouse heart transcriptome after myocardial infarction
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE104187 | GEO | 2018/05/07
REPOSITORIES: GEO
Similar Datasets
Project description:During myocardial infarction (MI), energy production decreases as hypoxia inhibits oxidative metabolism. Our lab has identified an ischemia-regulated alternative splicing event of the glycolytic enzyme pyruvate kinase (muscle, PKM), reducing PKM1 expression and increasing PKM2 expression. We hypothesized the upregulation of PKM2 aids in energy production to maintain heart function after MI. We utilized high-throughput sequencing to evaluate altered gene expression and identify pathways that may be regulated by PKM2.
2024-09-18 | GSE243668 | GEO
Project description:Background: Ischemic preconditioning (IPC), i.e., brief periods of ischemia, protect the heart from subsequent prolonged ischemic injury, and reduces infarction size. Myocardial stunning refers to transient loss of contractility in the heart after myocardial ischemia that recovers without causing permanent damage. The relationship between IPC and myocardial stunning remains incompletely understood. Purpose: The primary aim of this study was to examine the effects of IPC on the relationship between ischemia duration, stunning, and infarct size in an ischemia-reperfusion injury model. The secondary aim of the study was to examine to which extent the phosphoproteomic changes induced by IPC relate to myocardial contractile function. Methods: Rats were subjected to different durations of left anterior descending artery (LAD) occlusion, with or without preceding IPC. Echocardiograms were acquired at 4 and 48 hours to assess cardiac contraction in the affected myocardial segment. Reversible akinesia was defined as the presence of myocardial akinesia at 4 hours that resolved by 48 hours; and was considered to represent myocardial stunning. Infarction size was evaluated using triphenyl tetrazolium chloride staining. Phosphoproteomic analysis was performed in heart tissue from preconditioned and non-preconditioned animals using nano-liquid chromatography-mass spectrometry. Results: Reversible akinesia was observed in a majority of the rats that were subjected to IPC and subsequently exposed to ischemia of 13.5 or 15 minutes of ischemia (83.3% [n/N] and 66.6% [n/N] respectively). Among rats without IPC, who were exposed to either 10, 11, 12 or 13.5 minutes of ischemia, reversible akinesia was observed in 0% (n/N), 17% (2/12), 0% (n/N) and 0% (n/N) of rats (p<0.001). Phosphoproteomic analysis revealed significant differential regulation of 809 phosphopeptides between IPC and non-IPC groups, with significant associations with the sarcomere, Z-disc, and actin binding. Conclusion: Our study shows that IPC preferentially induces changes in phosphosites of proteins involved in myocardial contraction, and both increases the incidence of reversible post-ischemic myocardial stunning after ischemia-reperfusion injury and reduces infarction size.
2024-05-15 | PXD050441 | Pride
Project description:We established a rat model of myocardial Infarction by performing a surgical operation of left anterior descending coronary artery occlusion under sterie conditions. Wistar rats were previously randomly divided into 4 groups: control, ischemia, ischemia-propranolol, and non-ischemia-propranolol. Our data suggested that propranolol could reverse many microRNAs with too high or too low expression in the ischemia group versus control group.
2009-11-19 | GSE18129 | GEO
Project description:Affymetrix microarray analysis of molecular changes after myocardial infarction. Samples of heart tissue were analyzed after myocardial infarction from WT and reg3beta knock-out mice. Samples from scar tissue and samples adjacent to the scar were analyzed. In the experiment we primarily compared infarction zone of wild-type to infarction zone of knock-out animals, and remote zone of wild-type to remote zone of knock-outs.
2015-06-29 | E-MTAB-2561 | biostudies-arrayexpress
Project description:Ischemia reperfusion injury (IRI) following intervention for myocardial infarction remains an unmet clinical problem. Using an established mouse model, we demonstrated that IRI induces multiple cardiac cell linages to senescence. Senescence is is detrimental to recovery, as treatment with the senolytic navitoclax improves functional recovery.Here we are using SWATH-MS to investigate the molecular mechanisms responsible for the effect of navitoclax treatment.
2020-02-29 | MSV000085040 | MassIVE
Project description:MicroRNAs (miRNAs) are an important component of post-transcriptional regulation of gene expression. We hypothesized that early changes in miRNAs may be important for responses to cardiac injury. The goal of this study was to use high throughput sequencing to determine which miRNAs are altered in the initial response to ischemia after myocardial infarction.
2020-07-24 | GSE138141 | GEO
Project description:In the severity of myocardial infarction, Toll-like receptor (TLR) 9 plays a pivotal role in the inflammatory responses induced through damage-associated molecular patterns involving mitochondrial DNA and HMGB1. However, the therapeutic agents currently available for myocardial infarction substantially lack any association with the effects on immune responses. In this study, we applied a comprehensive drug discovery approach, which integrates in silico, in vitro, and in vivo processes, as well as determined therapeutic effects and mechanisms free from side effects. In an animal model of myocardial infarction, conditioned based on pharmacological properties, improved effects compared to the FDA-approved Rosuvastatin were detected. In summary, a small molecular inhibitor, ETA53 (endosomal Toll-like receptor antagonist 53), which selectively acts on TLR9 in nano-molar units, was developed. ETA53 was found to be effective for treating myocardial infarction caused by permanent ligation of the left anterior descending coronary artery, based on indicators such as cardiac function, inflammation, infarct size, and fibrosis. The results offered insights that varied from those of conventional drug development perspectives; consequently, the novel inhibitor may provide an alternative treatment with a mechanism different from that of the commercially available drugs for myocardial infarction.
2023-11-12 | GSE247311 | GEO
Project description:We established a rat model of myocardial Infarction by performing a surgical operation of left anterior descending coronary artery occlusion under sterie conditions. Wistar rats were previously randomly divided into 4 groups: control, ischemia, ischemia-propranolol, and non-ischemia-propranolol. Our data suggested that propranolol could reverse many microRNAs with too high or too low expression in the ischemia group versus control group. Wistar rats were initially anesthetized with pentobarbital (40 mg/kg, i.v.), which were previously randomly divided into 4 groups: control, ischemia (MI), ischemia-propranolol (MI-PRO), and non-ischemia-propranolol (NMI-PRO). The rat model of MI was established by performing a surgical operation of left anterior descending coronary artery occlusion under sterie conditions. Successful occlusion was confirmed by an increase in the amplitude of R wave of lead I during the first few seconds of each occlusion and elevation of S-T segment of lead II, and a 20-30% decline in the arterial blood pressure compared to the pre-ischemic values mesured by a previously installed ECG recorder (BL 420, ChengDu TME Technology Co, Ltd, ChengDu, China). Propranolol was administrated 2 months before the experiment with daily oral doses of 50 mg/kg. Hearts were quickly isolated after the rats were sacrificed and the ischemic zone of the left ventricle was prepared for the miRNA microarray experiment. Control and NMI-PRO animals underwent open chest procedures without coronary artery occlusion.
2010-06-19 | E-GEOD-18129 | biostudies-arrayexpress
Project description:Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients. ST-segment elevation myocardial infarction alters expression of several groups of genes. On admission, several genes and pathways that could be directly or indirectly linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability were affected (signaling of PPAR, IL-10, IL-6). Analysis at discharge highlighted specific immune response (upregulation of immunoglobulins). Highly significant and substantial upregulation of SOCS3 and FAM20 genes expression in the first 4-6 days of myocardial infarction in all patients is the most robust observation of our work Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1st day of myocardial infarction, after 4-6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease (CAD), without history of myocardial infarction. Gene expression analysis was performed with Affymetrix GeneChipM-BM-. Human Gene 1.0 ST microarrays and GCS3000 TG system.
2014-10-23 | E-GEOD-62646 | biostudies-arrayexpress
Project description:Coronary artery disease (CAD) remains a leading cause of death worldwide. Acute coronary syndromes (ACS) are the spectrum of diseases arising from coronary atherosclerotic plaque rupture, ranging from unstable angina (UA; clinical symptoms of cardiac ischemia without myocardial necrosis) to myocardial infarction (MI; clinical symptoms of cardiac ischemia with myocardial necrosis). We use microrray to identify changes in pathways following MI.This study examines mRNA expression levels in human whole blood at 7 and 30 days post ACS. Patients with MI are compared to those with UA (not healthy controls), thus focusing on differences in mRNA expression due to the acute clinical events rather than underlying atherosclerosis and its treatment.
2011-05-06 | GSE29111 | GEO