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Blood milieu in acute myocardial infarction reprograms human macrophages for trauma repair

ABSTRACT: Blood milieu in acute myocardial infarction reprograms human macrophages for trauma repair

PROVIDER: PRJNA890635 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21906863_1.fastq.gz	Fastqsanger.gz
	SRR21906863_2.fastq.gz	Fastqsanger.gz
	SRR21906864_1.fastq.gz	Fastqsanger.gz
	SRR21906864_2.fastq.gz	Fastqsanger.gz
	SRR21906865_1.fastq.gz	Fastqsanger.gz

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Blood milieu in acute myocardial infarction reprograms human macrophages for trauma repair

Project description:Acute myocardial infarction (AMI) is accompanied by a systemic trauma response that impacts on the whole body, including blood. In this study, we addressed whether macrophages, key players in trauma repair, sense and respond to these changes. For this, healthy human monocyte-derived macrophages were exposed to 20% human AMI (n=50) or control (n=20) serum and analyzed by transcriptional and multiparameter functional screening followed by network-guided data interpretation and drug repurposing. Results were validated in an independent cohort at functional level (n=47 AMI, n=25 control) and in a public dataset. AMI serum exposure resulted in an overt AMI signature, enriched in debris cleaning, mitosis, and immune pathways. Moreover, we identified gene networks associated with AMI and with poor clinical prognosis in AMI. Network-guided drug screening on the latter unveiled Prostaglandin E2 (PGE2) signaling as target for clinical intervention in detrimental macrophage imprinting during AMI trauma healing. Our results demonstrate pronounced context-induced macrophage reprogramming by the AMI systemic environment, to a degree decisive for patient prognosis. This offers new opportunities for targeted intervention and optimized cardiovascular disease risk management.

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

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

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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.

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Project description:Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients. ST-segment elevation myocardial infarction alters expression of several groups of genes. On admission, several genes and pathways that could be directly or indirectly linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability were affected (signaling of PPAR, IL-10, IL-6). Analysis at discharge highlighted specific immune response (upregulation of immunoglobulins). Highly significant and substantial upregulation of SOCS3 and FAM20 genes expression in the first 4-6 days of myocardial infarction in all patients is the most robust observation of our work Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1st day of myocardial infarction, after 4-6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease (CAD), without history of myocardial infarction. Gene expression analysis was performed with Affymetrix GeneChipM-BM-. Human Gene 1.0 ST microarrays and GCS3000 TG system.

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