MI: 1 and 7 days post-op
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE1957 | GEO | 2005/11/10
SECONDARY ACCESSION(S): PRJNA90905
REPOSITORIES: GEO
Similar Datasets
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
Project description:Male C57Bl/6 mice were randomized to undergo 5 days of i) a shiftwork protocol (10-hour light: 10-hour dark cycle) before myocardial infarction (MI) surgery, ii) a normal 12-hour light: 12-hour dark environment before MI surgery, iii) a normal 12-hour light: 12-hour dark environment and used as sham controls, or iv) a shiftwork protocol (10-hour light: 10-hour dark cycle) and used as sham controls. MI surgery was performed on the 5th day, after which all mice were returned to a normal 12-hour light: 12-hour dark cycle. Hearts were collected 24-hours post-MI at ZT06. The microarray approach allows the investigation of transcriptome-wide gene expression changes in hearts from mice on a shiftwork cycle or on a regular light:dark cycle before MI.
2018-11-30 | GSE123092 | GEO
Project description:Mice are 14 days post-mI/R (10 weeks old) on a C57Bl/6N background strain, hearts were collected at ZT15, following administration of saline placebo, sleeptime captopril (ZT01), or waketime captopril (ZT11) I.P. from day 7-14 post-mI/R. The microarray approach allows the investigation of gene expression changes of all genes in placebo vs. sleeptime vs. waketime vs. sham hearts.
2018-06-12 | GSE115568 | GEO
Project description:Bulk RNA expression profiles were captured from hearts of alpha7 nicotinic acetylcholine receptor (Chrna7) knockout (KO) and wild type (WT) mice that underwent myocardial infarction (MI) or sham (SH) surgery at postnatal day 1 and full ventricle collection at 7 days post-surgery
2021-09-28 | GSE184792 | GEO
Project description:Bulk RNA expression profiles were captured from hearts of Leucine-rich repeat containing protein 10 (Lrrc10) knockout (KO) and wild type (WT) mice that underwent myocardial infarction (MI) or sham (SH) surgery at postnatal day 1 and full ventricle collection at 7 days post-surgery
2023-07-10 | GSE221539 | GEO
Project description:In this project we explore the role of the master hypoxia regulator, Hypoxia inducible factor-1alpha (Hif-1a), in governing cardiac fibroblast (CF) function in homeostasis and following an acute ischaemic injury - myocardial infarction (MI). CF-specific Hif-1a conditional knockout (cKO) mice were generated by breeding Pdgfra-merCremer (PdgfraMCM/+) Cre recombinase driver mice with Hif-1a-floxed mice (Hif-1aflox/). In Hif-1afl/-; PdgfraMCM/+ progeny, Hif-1a could be conditionally deleted in adult CFs by tamoxifen (tam) administration. We also introduced a Cre-dependent R26tdTomato reporter allele allowing marking of Pdgfra+ CFs and their progeny. In this experiment, we first performed single-cell RNA sequencing (scRNA-seq) on tdTomato+ cells from the hearts of healthy cKO or heterozygous (HET) adult, male mice using the 10x Genomics Chromium system. We also performed scRNA-seq on tdTomato+/CD31-/CD45- cells from the hearts of cKO or HET mice at day-3 post-sham or -MI surgery.
2021-11-11 | E-MTAB-9583 | biostudies-arrayexpress
Project description:To explore the key lncRNAs involved in regulating essential pathophysiological processes of the adult heart, we performed microarray-based transcriptome profiling on mouse hearts 3 days and 14 days after myocardial infarction (MI) or sham surgery. Microarray analysis revealed a total of 7,339 differentially expressed transcripts in MI 3 days hearts compared to sham controls (FC≥2, p<0.05). Kyoto Encyclopedia of Genes and Genomes (KEGG) or Gene Ontology (GO) pathway analyses revealed that oxidative phosphorylation, ECM-receptor interaction, cell proliferation, and inflammatory responses were among the top dysregulated genes in MI hearts. Interestingly, 209 lncRNAs are upregulated and 543 lncRNAs are downregulated in MI 3 days hearts (FC≥2, p<0.05). Among these lncRNA transcripts, we found that 8 lncRNAs are mostly upregulated and 6 lncRNAs mostly downregulated (FC≥2, p<0.05), whereas the expression level of the AK048087 transcript was increased by 25 fold and lncRNA AK034241 appears to be the most downregulated lncRNA.
2020-11-14 | GSE161427 | GEO
Project description:We have earlier observed that upon myocardial infarction, pre-existing coronary arteries give rise to new collateral arteries via Artery Reassembly (AR) in neonatal mice, but not in adults. To understand this age dependent phenomenon, Gja5 (Cx40), an established artery endothelial cell marker, was used to lineage trace artery cells with TdTomato expression. For the neonatal mice, Tamoxifen was induced at postnatal (P)0, Myocardial Infarction (MI)/sham was performed at P2 and hearts were harvested at either P4 or P5. Whereas, for the adults, mice aged ~2months were used. Tamoxifen was induced at Day (D)0, MI/sham was performed at D2 and hearts were harvested at either D9 or D11. Ventricles from hearts were digested and FACS sorted for DAPI-, Ter199- and TdTomato+ cells.
2023-07-05 | GSE210307 | GEO
Project description:Rational: We previously reported evidence of endothelial to mesenchymal transition (EndMT) and fibrosis in mitral valve (MV) leaflets at two to six months post-myocardial infarction (MI) in sheep. The onset of these changes and the mechanism of their instigation are not known. Early modulation of EndMT and fibrosis in MV leaflets may limit the development of ischemic mitral regurgitation (IMR) and heart failure. H Objective: To test the hypothesis that circulating molecules present in plasma within days after MI incite EndMT and fibrotic processes in MV leaflets. Method and Results: Ovine MVs harvested 8-10 days after inferior MI (IMI) showed an increase in MV thickness by histology and onset of EndMT, shown by increased CD31/α-smooth muscle actin (α-SMA)+ cells in post-MI MV leaflets (10.5±6.9%) versus sham (2.6±4%). In vitro, post-MI plasma induced EndMT and pro-fibrotic markers and enhanced migration of primary mitral valve endothelial cells (VECs). In contrast, sham plasma did not, despite the presence of TGFβ2 at levels known to induce EndMT in VECs (2 ng/ml). Analysis of sham versus post-MI plasma using a cytokine array revealed a significant drop in the Wnt signaling antagonist secreted frizzled-related protein 3 (sFRP3) in post-MI plasma compared to sham plasma, which was confirmed by ELISA. Addition of recombinant sFRP3 to post-MI plasma reversed its EndMT-inducing effect on mitral VECs, measured by restored VE-cadherin, reduced α-SMA, and reduced TGFβ1-3 expression. Extracellular signal related kinase 1/2 and SMAD2/3 phosphorylation were increased in mitral VEC by post-MI plasma, and both were blocked by supplementing the post-MI plasma with sFRP3. RNA-seq analysis of mitral VECs exposed to post-MI versus sham plasma for 24 hours showed upregulated forkhead box M1 (FOXM1), a transcription factor previously shown to drive fibrosis. FOXM1 was co-localized with CD31 in MV leaflets obtained from sheep at 8-10 days post-MI, which suggests FOXM1 may be linked to EndMT initiation. Blocking FOXM1 with Siomycin A (Sio A) reduced EndMT and pro-fibrotic transcripts in post-MI plasma treated mitral VECs. Finally, post-MI plasma-induced and TGFβ-induced FOXM1 was downregulated by sFRP3. Conclusions: Reduced sFRP3 in post-MI plasma appears to facilitate the onset of TGFβ-driven EndMT and fibrosis in mitral VECs by increasing the transcription factor FOXM1. Restoring sFRP3 levels and/or inhibiting FOXM1 may provide new strategies to minimize maladaptive changes that occur in the MV due to MI.
2022-01-15 | GSE182696 | GEO
Project description:In this study, we used a cardiac-specific, inducible expression system to activate YAP in adult mouse heart. Activation of YAP in adult heart promoted cardiomyocyte proliferation and did not deleteriously affect heart function. Furthermore, YAP activation after myocardial infarction (MI) preserved heart function and reduced infarct size. Using adeno-associated virus subtype 9 (AAV9) as a delivery vector, we expressed human YAP in the murine myocardium immediately after MI. We found that AAV9:hYAP significantly improved cardiac function and mouse survival. AAV9:hYAP did not exert its salutary effects by reducing cardiomyocyte apoptosis. Rather, we found that AAV9:hYAP stimulated adult cardiomyocyte proliferation. Gene expression profiling indicated that AAV9:hYAP stimulated cell cycle gene expression, enhanced TGFβ-signaling, and activated of components of the inflammatory response.Cardiac specific YAP activation after MI mitigated myocardial injury after MI, improved cardiac function and mouse survival. These findings suggest that therapeutic activation of hYAP or its downstream targets, potentially through AAV-mediated gene therapy, may be a strategy to improve outcome after MI. Three groups were involved in this study: sham group, AAV9:Luci+MI group and AAV9-YAP+MI group. Each group contained three biological replicates. The sham group had neither myocardial infarction nor AAV injection. The AAV9:Luci +MI(L for brief) group had myocardial infarction and injected with AAV9:Luic. The AAV9:hYAP+MI(YAP for brief) group had myocardial infarction and injected with AAV9:hYAP. 5 days after MI and AAV injection, the heart apexes were collected and the total RNA were isolated for microarray analysis.
2014-05-26 | E-GEOD-54612 | biostudies-arrayexpress