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.
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
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
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.
Project description:Prognosis after myocardial infarction (MI) varies greatly depending of the extent of damaged area and the management of biological processes during recovery. Reportedly, the inhibition of the pro-inflammatory S100A9 reduces myocardial damage after MI. We hypothesize that S100A9 blockade induces changes of major signaling pathways implicated in post-MI healing. The S100A9 blocker (ABR-23890) was given for 3 days after coronary ligation. At 3- and 7-days post-MI, ventricle samples were analyzed versus control and sham-operated mice. Blockade of S100A9 modulated the expressed proteins involved in five biological processes: leu-kocyte cell-cell adhesion, regulation of muscle cell apoptotic process, regulation of intrinsic apoptotic signaling pathway, sarcomere organization and cardiac muscle hypertrophy. The blocker induced regulation of 36 proteins interacting with or targeted by the cellular tumor antigen p53, prevented myocardial compensatory hypertrophy, and reduced cardiac markers of post-ischemic stress. The blockade effect was prominent at day 7 post-MI when the quantitative features of ventricle proteome were closer to controls.
Project description:Purpose: rHCI hydrogel injection improves cardiac function within 2 days of treatment in a mouse model of myocardial infarction. The goal of this study was to determine the differences in gene expression with rHCI hydrogel injection post-myocardial infarction. Methods: Total RNA was isolated from left ventricle tissue of samples and mRNA stranded libraries were prepared and sequenced in Illumina NovaSeq 6000 with a depth of 50 million reads per sample. Differential expression analysis of aligned reads was done to compared gene expression between PBS vs. rHCI, PBS vs. sham, and rHCI vs. sham comparisons. Results: Differentially expressed genes between sham and PBS as well as rHCI and PBS showed known gene signatures of myocardial infarction. Seven differentially expressed genes were detected with rHCI hydrogel injection compared to PBS. Conclusions: The target gene ERDR1 that is downregulated with rHCI injection led to discovery of changes in cardiomyocyte apoptosis and reduction of oxidative stress adducts with rHCI injection post-myocardial infarction.
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.
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.
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.
