IlEucMixx
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB53246 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR9820271_1.fastq.gz | Fastqsanger.gz | |||
| ERR9820271_2.fastq.gz | Fastqsanger.gz | |||
| ERR9820272_1.fastq.gz | Fastqsanger.gz | |||
| ERR9820272_2.fastq.gz | Fastqsanger.gz | |||
| ERR9836425.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:Myocardial infarction (MI) is the leading cause for hear failure (HF). Following MI, the non-infarcted region of left ventricle (LV) is critical for maintaining heart function, and disruption of the LV contributes greatly to post-MI HF. Transcriptomic profiling by high-throughput sequencing was performed in a chronic HF pig model, to explore the molecular changes in the post-MI LV related to cardiovascular deterioration. Samples were taken from heart tissue of MI-induced pigs and from control pigs not subjected to MI. Regions of the heart where samples were taken included the site of ischemia (LV ischemia), area bordering ischemia (LV border), area remote to ischemia (LV remote) and the right ventricle (RV).
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Project description:Monocytes play a central role in the inflammatory response that follows acute myocardial infarction (MI). In order to study phenotypic adaptation of this cell type, we investigated patterns of monocyte gene expression in circulating monocytes at various stages of MI. Circulating monocytes were isolated from venous blood of MI patients at three time points: t1: within 6 hours after onset of chest pain (acute phase), t2: 3 days after MI (subacute phase), t3: 90 days after MI (chronic phase). For comparison, we studied a control group (n=21, data to be submitted later) with stable coronary artery disease. Using this transcriptomic analysis, we aimed to provide a more comprehensive reference of monocyte biology following acute MI and to aid in the identification of novel pathways and genes influencing the course of MI.
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