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RNA sequencing of rodent myocardial tissue when subjected to a myocardial infarction (MI) or an MI and a surgical device (TRD) for 12 weeks.

ABSTRACT: RNA sequencing of rodent myocardial tissue when subjected to a myocardial infarction (MI) or an MI and a surgical device (TRD) for 12 weeks.

PROVIDER: PRJNA628505 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11611400_1.fastq.gz	Fastqsanger.gz
	SRR11611400_2.fastq.gz	Fastqsanger.gz
	SRR11611401_1.fastq.gz	Fastqsanger.gz
	SRR11611401_2.fastq.gz	Fastqsanger.gz
	SRR11611402_1.fastq.gz	Fastqsanger.gz

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RNA sequencing of rodent myocardial tissue when subjected to a myocardial infarction (MI) or an MI and a surgical device (TRD) for 12 weeks.

Project description:Purpose: The goal of this study is to compare mRNA related cellular pathways associated with a myocardial infarction (MI) with a surgical device to prevent cardiac remodeling compared to an MI only Conclusions: RNA sequencing revealed an activation of multiple cellular pathways with the device group.

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Expression data for patients with myocardial infarction (MI) vs healthy patients

Project description:Myocardial infarction (MI) is one of the most severe manifestations of coronary artery disease (CAD) and the leading cause of death from non-infectious diseases worldwide. It is known, that the central component of CAD pathogenesis is a chronic vascular inflammation. However, the mechanisms underlying the changes that occur in T, B and NK-lymphocytes, monocytes and other immune cells during CAD and MI are still poorly understood. One of those pathogenic mechanisms might be the dysregulation of intracellular signaling pathways in the immune cells. In the present study we performed a transcriptome profiling in peripheral blood mononuclear cells of MI patients and healthy individuals. The machine learning algorithm was then used to search for MI-associated signatures, that could reflect the dysregulation of intracellular signaling pathways and be assisted in MI diagnosis and/or prognosis. ADAP2, KLRC1, MIR21, PDGFD and CD14 genes were identified as the most important signatures for the classification model with L1-norm penalty function. The classifier output quality was equal to 0.911 by Receiver Operating Characteristic metric on test data. These results were validated on two independent open GEO datasets.

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mRNA Expression data from murine hearts subjected to ligation of the left anterior descending coronary artery (myocardial infarction, MI model) or sham surgery (SH)

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.

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Cardiac-specific YAP activation improve cardiac function and survival in an experimental murine MI model

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.

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mRNA Expression Data from Murine Hearts of Shiftwork MI, Normal MI and Sham Wildtype Mice at 24-hours Post-MI

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