Myocardial infarction time series single cell RNA-Seq
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ABSTRACT:
PROVIDER: PRJEB32278 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We performed time-series single-cell RNA-seq analysis of blood CD11b+ cells and of the inflammatory infiltrate in the heart of C57BL/6J male mice in a model of permanent myocardial infarction.
2020-08-18 | GSE135310 | GEO
Project description:The outcome of cardiac repair post myocardial infarction is highly dependent on the balance between inflammation and fibrosis, which can lead to adverse ventricular remodeling and failure or early cardiac rupture. In order to profile the dynamic response of the interstitium to cardiac ischemic injury, we performed unbiased single cell RNA Sequencing (scRNAseq) on cardiac interstitial cells at homeostasis and 1, 3, 5, 7, 14, 28 days post-injury using transgenic mice on C57bl/6j background (B6), expressing ZsGreen under the control of the epicardial marker Wt1 (Wt1Cre;RosaZsgreenf/+). About 38,600 cells were captured using the 10xChromium technology. To gain insights on how cell composition and transcriptome can affect the predisposition to cardiac rupture, we compared the data on B6 background with 129S1/SvlmJ (129) mice sham and d3 post-MI (time point proceeding the rupture), capturing about 13,000 additional cells.
2020-03-04 | E-MTAB-7895 | biostudies-arrayexpress
Project description:Time series single cell transcriptomics of cardiac inflammation after myocardial infarction in mice
| PRJNA558375 | ENA
Project description:We generated a single cell accessibility atlas from different time points after murine myocardial infarction as an important source for the field.
2023-02-01 | GSE166008 | GEO
Project description:We applied single-cell transcriptomics to identify cellular and molecular heterogeneity in distinct heart cell populations in myocardial infarction versus sham surgery mice.
2019-09-02 | GSE136088 | GEO
Project description:Myocardial infarction (MI) is one of the deadliest diseases in the world, and the changes at the molecular level after MI and the DNA methylation features are not clear. Understanding the molecular characteristics of the early stages of MI is of significance for the treatment of the disease. In this study, RNA-seq and MeDIP-seq were performed on heart tissue from mouse models at multiple time points (0 h, 10 min,1 h, 6 h, 24 h and 72 h) to explore genetic and epigenetic features that influence MI progression. Analysis based on a single point in time, the number of differentially expressed genes (DEGs)and differentially methylated regions (DMRs)increased with the time of myocardial infarction, using 0 h as a control group. Moreover, within 10 minutes of MI onset, the cells are mainly in immune response, and as the duration of MI increases, apoptosis begins to occur. Analysis based on time series data, the expression of 1012 genes was specifically downregulated, and these genes were associated with energy metabolism. The expression of 5806 genes was specifically upregulated, and these genes were associated with immune regulation, inflammation and apoptosis. 14 transcription factors were identified in the genes involved in apoptosis and inflammation, which may be potential drug targets. Analysis based on MeDIP-seq combined with RNA-seq methodology, focused on methylation at the promoter region. GO revealed that the downregulated genes with hypermethylation at 72 h were enriched in biological processes such as cardiac muscle contraction. In addition, the upregulated genes with hypomethylation at 72 h were enriched in biological processes, such as cell-cell adhesion, regulation of the apoptotic signalling pathway and regulation of angiogenesis. Among these genes, the Tnni3 gene was also present in the downregulated model. Hypermethylation of Tnni3 at 72 hours after MI may be an important cause of exacerbation of MI.
2022-06-23 | GSE206281 | GEO
Project description:Myocardial infarction (MI) is one of the deadliest diseases in the world, and the changes at the molecular level after MI and the DNA methylation features are not clear. Understanding the molecular characteristics of the early stages of MI is of significance for the treatment of the disease. In this study, RNA-seq and MeDIP-seq were performed on heart tissue from mouse models at multiple time points (0 h, 10 min,1 h, 6 h, 24 h and 72 h) to explore genetic and epigenetic features that influence MI progression. Analysis based on a single point in time, the number of differentially expressed genes (DEGs)and differentially methylated regions (DMRs)increased with the time of myocardial infarction, using 0 h as a control group. Moreover, within 10 minutes of MI onset, the cells are mainly in immune response, and as the duration of MI increases, apoptosis begins to occur. Analysis based on time series data, the expression of 1012 genes was specifically downregulated, and these genes were associated with energy metabolism. The expression of 5806 genes was specifically upregulated, and these genes were associated with immune regulation, inflammation and apoptosis. 14 transcription factors were identified in the genes involved in apoptosis and inflammation, which may be potential drug targets. Analysis based on MeDIP-seq combined with RNA-seq methodology, focused on methylation at the promoter region. GO revealed that the downregulated genes with hypermethylation at 72 h were enriched in biological processes such as cardiac muscle contraction. In addition, the upregulated genes with hypomethylation at 72 h were enriched in biological processes, such as cell-cell adhesion, regulation of the apoptotic signalling pathway and regulation of angiogenesis. Among these genes, the Tnni3 gene was also present in the downregulated model. Hypermethylation of Tnni3 at 72 hours after MI may be an important cause of exacerbation of MI.
2022-06-23 | GSE206280 | 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:Background and Aims: It is known that inflammatory processes are activated in heart failure, but the regulation of cytokines and their role in the pathogenesis of the disease are not well understood. To address this issue, we have performed microarray analysis of non-infarcted left ventricular tissue from mice at various time-points after myocardial infarction. Methods: Molecular alterations in myocardial tissue were measured 3, 5, 7 and 14 days after induced infarction by using cDNA microarrays. Sham operated mice served as controls. Altered gene transcriptions were verified by real-time polymerase chain reaction. Attention focused on genes encoding cytokines which had not previously been assigned a role in heart failure development. Results: The highest number of regulated genes was found at day 5 post myocardial infarction, and 22 genes encoding cytokines were identified as being regulated. Several of the identified genes encoding cytokines have not previously been associated with HF, and among those fractalkine showed strongest up-regulation. Keywords: Disease state analysis, time course
2008-09-25 | GSE6580 | GEO
Project description:Analysis of time series gene expression and DNA methylation reveals the molecular features of myocardial infarction progression
| PRJNA849947 | ENA