Expression data from mouse heart three days after myocardial infarction
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PROVIDER: PRJNA664127 | ENA |
REPOSITORIES: ENA
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Project description:Identification of the genes whose expresion levels are changed by the operation of myocardial infarction in C57BL/6J mice
2022-12-19 | GSE158157 | GEO
Project description:Background: There are critical molecular mechanisms that can be activated to induce myocardial repair and in humans this is most efficient during fetal development. The timing of heart development in relation to birth and the size/electrophysiology of the heart are similar in humans and sheep, providing a model to investigate the repair capacity of the mammalian heart and how this can be applied to adult heart repair. Methods: Myocardial infarction was induced by ligation of the left anterior descending coronary artery in fetal (105d gestation when cardiomyocytes are proliferative) and adolescent sheep (6 months of age when all cardiomyocytes have switched to an adult phenotype). An ovine gene microarray was used to compare gene expression in sham and infarcted (remote, border and infarct areas) cardiac tissue from fetal and adolescent hearts. Results: The gene response to myocardial infarction was less pronounced in fetal compared to adolescent sheep hearts and there were unique gene responses at each age. There were also region-specific changes in gene expression between each age, in the infarct tissue, tissue bordering the infarct, and tissue remote from the infarction. In total, there were 880 genes that responded to MI uniquely in the adolescent samples compared with 170 genes in the fetal response, as well as 742 overlap genes that showed concordant direction of change responses to infarction at both ages. Conclusions: In response to myocardial infarction, there were specific changes in genes within pathways of mitochondrial oxidation, muscle contraction, and haematopoietic cell lineages, suggesting that the control of energy utilisation and immune function are critical for effective heart repair. The more restricted gene response in the fetus may be an important factor in its enhanced capacity for cardiac repair.
2020-01-30 | GSE144509 | 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:We demonstrate an age-independent loss of type H bone endothelium in heart failure after myocardial infarction in both mice and in humans. Using single-cell RNA sequencing, we delineate the transcriptional heterogeneity of human bone marrow endothelium showing increased expression of inflammatory genes, including IL1B and MYC, in ischemic heart failure. Endothelial-specific overexpression of MYC was sufficient to induce type H bone endothelial cells, whereas inhibition of NLRP3-dependent IL-1 production partially prevents the post-myocardial infarction loss of type H vasculature in mice.
2021-05-13 | E-MTAB-10448 | biostudies-arrayexpress
Project description:We demonstrate an age-independent loss of type H bone endothelium in heart failure after myocardial infarction in both mice and in humans. Using single-cell RNA sequencing, we delineate the transcriptional heterogeneity of human bone marrow endothelium showing increased expression of inflammatory genes, including IL1B and MYC, in ischemic heart failure. Endothelial-specific overexpression of MYC was sufficient to induce type H bone endothelial cells, whereas inhibition of NLRP3-dependent IL-1 production partially prevents the post-myocardial infarction loss of type H vasculature in mice.
2021-05-11 | E-MTAB-10432 | biostudies-arrayexpress
Project description:We tested it in an animal model of myocardial infarction to ensure whether early initiation of dapagliflozin (DAPA), or different orders of combination with sacubitril-valsartan would result in a greater improvement of heart function than sacubitril-valsartan alone in post-myocardial infarction heart failure.
2023-04-13 | GSE229147 | GEO
Project description:To test the mechanism by which IGF1 is cardioprotective, we performed single cell RNA sequencing on myeloid cells isolated from the heart 3 days after myocardial infarction of mice with and without IGF1 treatment. Myocardial infarction was induced in C57Bl6/J mice by 45 min occlusion of the left anterior descending artery followed by 3 days of reperfusion. Animals of the IGF1 group (n=3) received 40 ng/g mature recombinant IGF1 subcutaneously as bolus at the beginning of reperfusion. In addition, IGF1 (1 µg/g/d) was administered continuously during reperfusion using micro-osmotic pumps (Alzet, 1003D) that were implanted subcutaneously. Control mice received vehicle (0.1% BSA). After 3 days hearts were digested and CD45+CD11b+ cells were isolated using FACS cell sorting. Each sample contained cells containing 1 control and 1 IGF1 treated mouse, labeled with TotalSeq hashtags. 16000 cells were used as input for the single-cell droplet libraries generation for each sample.
2023-12-31 | E-MTAB-11590 | 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:The use of anthracycline antibiotics such as doxorubicin (DOX) has greatly improved the mortality and morbidity of cancer patients. However, the associated risk of cardiomyopathy has limited their clinical application. DOX-associated cardiotoxicity is irreversible and progresses to heart failure (HF). For this reason, a better understanding of the molecular mechanisms underlying these adverse cardiac effects is essential to develop improved regimes that include cardioprotective strategies. MicroRNAs (miRNAs) are short non-coding RNAs that are able to post-trascriptionally regulate gene expression. MiRNAs have been demonstrated to be involved in both cancer and cardiovascular disease. Therefore, we were interested in unveiling the potential role of miRNAs in chemotherapy-induced HF. We used a combination of three different models to recreate this cardiac toxicity (acute in vitro DOX treatment, DOX-induced HF in vivo and a myocardial infarction -MI- leading to failure model) to study the pattern of dysregulated miRNAs. Using RNA from all three conditions, miRNA microarray profiling was performed and a common miRNA signature was identified. Interestingly, these dysregulated miRNAs have been previously identified as involved in the failing heart. Our results suggest that DOX is able to alter the expression of miRNAs implicated in HF, in vitro as well as in vivo. The present study is a microRNA profiling of the damaged cardiac muscle (cardiomyocyte cell population), following either myocardial infarction (MI) induction or doxorubicin (DOX) treatment. Two DOX-treated models were included: ARC exposed to DOX in vitro and a validated DOX-induced heart failure model generated by repeated administration of DOX injections.
2013-01-29 | E-GEOD-36239 | biostudies-arrayexpress
Project description:Differential gene responses three days following infarction in the fetal and adolescent sheep heart
| PRJNA603845 | ENA