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Systemic environment in acute myocardial infarction programs human macrophages for trauma repair

ABSTRACT: In this study human primary monocyte-derived macrophages from healthy volunteers (pool of 6-8 donors) were exposed for 24 h to a 1:5 dilution of human patient serum. Patient sera were obtained either from control patients (n=20) or patients suffering an acute myocardial infarction (AMI, n=47, selected from POSTEMI trial, S. Limalanathan et al. J Am Heart Assoc 2014). All exposed macrophages were analyzed by RNA sequencing. The study revealed that macrophages significantly alter their gene expression profile in response the AMI-serum exposure, and adapt phagocytic, metabolic and cell cycling programs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE172270 | GEO | 2022/12/18

REPOSITORIES: GEO

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Project description:Whole-genome gene expression analysis has been successfully utilized to diagnose, prognosticate, and identify potential therapeutic targets for cardiovascular disease. However, the utility of this approach to identify outcome-related genes and dysregulated pathways following first-time myocardial infarction (AMI) remains unknown and may offer a novel strategy to detect affected expressome networks that predict long-term outcome. Whole-genome microarray and targeted cytokine expression profiling on blood samples from normal cardiac function controls and first-time AMI patients within 48-hours post-MI revealed expected differential gene expression profiles enriched for inflammation and immune-response pathways in AMI patients. To determine molecular signatures at the time of AMI that could prognosticate long-term outcomes, transcriptional profiles from sub-groups of AMI patients with (n=5) or without (n=22) any recurrent events over an 18-month follow-up were compared. This analysis identified 559 differentially expressed genes. Bioinformatic analysis of this differential gene set for associated pathways revealed 1) increasing disease severity in AMI patients is associated with a decreased expression of the developmental epithelial-to-mesenchymal transition, and 2) modulation of cholesterol transport genes that include ABCA1, CETP, APOA1, and LDLR is associated with clinical outcome. In conclusion, differentially regulated genes and modulated pathways were identified that predicted recurrent cardiovascular outcomes in first-time AMI patients. This cell-based approach for risk stratification in AMI warrants a larger study to determine the role of metabolic remodeling and regenerative processes required for optimal outcomes. A validated transcriptome assay could represent a novel, non-invasive platform to anticipate modifiable pathways and therapeutic targets to optimize long-term outcome for AMI patients. The overall experimental design includes blood samples from 21 control and 31 myocardial infaction patient groups. Among the 31patients, 5 patients have recurrent events. Microarray were peformed on the blood samples and comparisons of control vs patient and patients with recurrent events vs patients without recurrent events were performed to identify differential genes related to disease or patients groups with recurrent events for the following bioinformatic analysis.

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Systemic environment in acute myocardial infarction programs human macrophages for trauma repair

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