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The proteins detection in the Early Stage of Myocardial Infarction

ABSTRACT: Eight-week-old mice were divided into six groups: sham group, 10min after MI, 1h after MI, 6h after MI, 24h after MI and 72h after MI. Myocardial infarction was performed by ligating the proximal left anterior descending coronary artery. Then the infarction myocardial tissue was taken for DIA protein indentification.

ORGANISM(S): Mus Musculus

SUBMITTER: Wenju Liu

PROVIDER: PXD020193 | iProX | Sun Jul 05 00:00:00 BST 2020

REPOSITORIES: iProX

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Pyroptosis inhibition improves the symptom of acute myocardial infarction.

Liu Wenju W Shen Junwei J Shen Junwei J Li Yanfei Y Wu Jiawen J Luo Xiaoli X Yu Yuanyuan Y Zhang Yuhan Y Gu Liang L Zhang Xiaobai X Jiang Cizhong C Li Jue J

Cell death & disease 20210916 10

Acute myocardial infarction (AMI), the leading cause of mortality worldwide, is a rapidly developing and irreversible disease. Therefore, proper prompt intervention at the early stage of AMI is crucial for its treatment. However, the molecular features in the early stage have not been clarified. Here, we constructed mouse AMI model and profiled transcriptomes and proteomes at the early stages of AMI progress. Immune system was extensively activated at 6-h AMI. Then, pyroptosis was activated at 2 ...[more]

PMID: 34531373

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Multi-omics profiling of mouse myocardial infarction

Project description:Myocardial infarction (MI), the most severe manifestation of coronary artery disease, is a multifactorial pathophysiologic process. Here, we constructed a MI mouse model through ligation of the proximal left anterior descending coronary artery. Then we detected and analysed multi-omics (transcriptome and proteome) at different time points (Control, 10 mininte, 1 hour, 6 hour, 24 hour and 72 hour) after MI. Immune-related pathway, pyroptosis pathway, and autophagy pathway r were significantly increased after MI.

2021-09-14 | GSE153494 | GEO

Regulation of gene expression with thyorid hormone in rats with myocardial infarction

Project description:Thyroid hormone improves left ventricular remodeling and cardiac performance after myocardial infarction (MI), but the molecular basis is unknown. This study was designed to detect gene expression changes in left ventricular non-infarcted areas at 4 weeks following myocardial infarction with and without thyroid hormone treatment. The results suggest that altered expression of genes for molecular function and biological process may be involved in the beneficial effects of thyroid hormone treatment following myocardial infarction in rats. MI was produced by ligation of the left anterior descending coronary artery in female SD rats. Rats were divided into the following groups: (1) Sham MI, (2) MI, and (3) MI+T4 treatment (T4 pellet 3.3mg, 60 days release, implanted subcutaneously immediately following MI). Four weeks after surgery, total RNA was isolated from left ventricular non-infarcted areas for microarray analysis using the Illumina RatRef-12 Expression BeadChip Platform.

2012-04-30 | E-GEOD-35088 | biostudies-arrayexpress

mRNA Expression data from murine hearts subjected to ligation of the left anterior descending coronary artery (myocardial infarction, MI model) or sham surgery (SH)

Project description:The left anterior descending coronary artery permanent ligation model of myocardial infarction was used to study the time of day differences in genetic responses post-MI between sleep-time MI, wake-time MI, wake-sham and sleep-sham mouse hearts. The micorarray approach allows the investigation of gene expression changes of all genes in sleep-time MI vs. wake-time MI vs. sham hearts.

2018-08-06 | GSE71906 | GEO

Cardiopoietic stem cell therapy restores infarction-altered cardiac proteome

Project description:Cardiopoietic stem cells are in advanced clinical testing for ischemic heart failure. To profile their uncharted molecular influence on recipient hearts, systems proteomics was applied in a chronic murine model of infarction randomized with and without human cardiopoietic stem cell treatment. Four biological replicates are included from each of three separate groups, Control (Ctrl, n=4), myocardial infarction without treatment (MI, n=4), and MI with cardiopoietic stem cell treatment (CP, n=4). Athymic nude male mice (2-3 months of age) underwent left anterior descending coronary artery ligation (70-min occlusion followed by reperfusion). ST elevation on the electrocardiogram confirmed MI. Four weeks post-MI, animals were randomized into cohorts without (MI, n=4) or with (CP, n=4) cell therapy. Human CP cells were generated from bone marrow derived mesenchymal stem cells using an established cardiopoiesis protocol. Media (15 µL), with or without CP cells (600,000 cells/heart), were epicardially delivered in infarcted left ventricles.

2020-03-23 | PXD017381 | Pride

MicroRNA Expression in Rat Myocardial Infarction intervened by propranolol

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

microRNA data from mice hearts of 21 days post myocardial infarction versus sham control

Project description:microRNAs control cardiac remodeling post myocardial infarction, though the cellular and molecular mechanisms remain unclear. We used microarrays to examine microRNA profiles in mice hearts 21 days after ligation of left anterior descending coronary artery (LAD) versus sham control.

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miRNA expression data from the hearts of murine myocardial infarction model

Project description:Sexual dimorphisms are well recognized in various cardiac diseases, including myocardial infarction (MI). MI develops later in women, but once established, it contributes more persistent symptoms and higher mortality than in men. Similar observations have been reported in murine model of MI. Although mRNA-level sexual dimorphism of MI have been reported, whether miRNA transcriptome also confers such dimorphism remains unknown. Comprehensive understanding of the mRNA- and miRNA-level genetic programs underlying the heart sexual dimorphisms will expectedly improve clinical outcome by facilitating the development of gender specific treatment strategies. Here, by conducting miRNA microarray analysis of murine MI model samples, we set out to characterize the heart sexual dimorphisms at the level of miRNA transcriptome The left anterior descending (LAD) coronary artery of mice aged 10 weeks was surgically ligated to create extensive MI. The ventricular septum of the areas at risk of ischemia was sampled on post-operative day 28. Total RNA was extracted using Sepasol solution (Sepasol-RNA I super G, nakalai tesque, Japan), and microarray analysis was performed using Affymetrix GeneChipÂ® miRNA 3.0 Arrays

2016-01-07 | E-GEOD-76592 | biostudies-arrayexpress

Transcriptional profiling of left ventricle and peripheral blood cells in rats with post-myocardial infarction

Project description:Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). It is of great clinical importance to understand the molecular mechanisms that trigger transition from compensated LV injury to HF and to identify relevant diagnostic biomarkers. In this study, we performed transcriptional profiling of LVs in rats with a wide range of experimentally induced infarct sizes and of peripheral blood mononuclear cells (PBMCs) in animals that developed HF. We used microarrays to investigate gene expression in the left ventricle (LV) accompanying myocardial infarction and concomitant heart failure (HF) in a well validated model of post-infarcted heart failure and to evaluate their reflection in peripheral blood mononuclear cells (PBMCs) Myocardial infarction (MI) was induced in male Wistar rats by ligation of the proximal left coronary artery. The sham-operated group (control group) was subjected to the same protocol, except that the suture was not tied around the proximal left coronary artery. Sham-operated rats (n=6) and rats with small (n=6), moderate (n=6), and large (n=5) MI size were included into the experiment two months after the operation. Then, left ventricules and blood samples were obtained for RNA extraction and hybridization on Affymetrix microarrays. Microarrays were used to compare the LV and PBMCs transcriptomes of control and experimental animals. The development of heart failure was estimated by echocardiography and catheterization.

2013-11-15 | E-GEOD-47495 | biostudies-arrayexpress

MicroRNA Expression in Rat Myocardial Infarction intervened by propranolol

2009-11-19 | GSE18129 | GEO

Evaluating the effects of cardiac telomerase re-activation after myocardial infarction in adult mice

Project description:Coronary heart disease is a main cause of death in the developed world and treatment success remains modest with high mortality rates within one year after myocardial infarction (MI). Thus, new therapeutic targets and effective treatments are necessary. Short telomeres are risk factors for age-associated diseases including heart disease. Here, we address the potential of telomerase (Tert) activation in prevention of heart failure after MI in adult mice. We use adeno-associated viruses for cardiac-specific Tert expression in a mouse model of MI. We find that upon MI, hearts expressing Tert show attenuated cardiac dilation, improved ventricular function and smaller infarct scars concomitant with increased mouse survival by 17% compared to controls. Furthermore, Tert treatment results in elongated telomeres, increased numbers of Ki67 and pH3-positive cardiomyocytes and a gene expression switch towards a regeneration signature of neonatal mice. Our work highlights telomerase activation as a novel therapeutic strategy to prevent heart failure after MI. Mice of one year of age were left untreated (control) or injected with 5*10^11 adeno associated viruses particles of serotype 9 (AAV9) that carry either en empty expression cassette or express telomerase under control of the CMV promoter. Virus injected mice then underwent myocardial infarction induced through permenant left anterior descending artery (LAD) ligation. Mice that survived for six weeks after LAD ligation were sacrificed and 4 hearts per group (AAV9-empty or AAV9-Tert) and 3 control hearts (no virus treatment, no ligation) were subjected to total RNA isolation for micro array analysis.

2014-12-15 | E-GEOD-62973 | biostudies-arrayexpress

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