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Effect of depletion of the serine protease inhibitors (serpina3n) on gene expression in cardiac fibroblasts after myocardial injury (MI) in rodent models

ABSTRACT: Effect of depletion of the serine protease inhibitors (serpina3n) on gene expression in cardiac fibroblasts after myocardial injury (MI) in rodent models

PROVIDER: PRJNA991654 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25154640_1.fastq.gz	Fastqsanger.gz
	SRR25154640_2.fastq.gz	Fastqsanger.gz
	SRR25154641_1.fastq.gz	Fastqsanger.gz
	SRR25154641_2.fastq.gz	Fastqsanger.gz
	SRR25154642_1.fastq.gz	Fastqsanger.gz

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Effect of depletion of the serine protease inhibitors (serpina3n) on gene expression in cardiac fibroblasts after myocardial injury (MI) in rodent models

Project description:To investigate the function of serpina3n in cardiac fibroblast. Serpina3n is significantly upregulated after myocardial injury in rodent models. The depletion of serpina3n causes heart function weakening in rodent models.

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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.

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Knockdown of serine protease PRSS23 decreased FGF2 expression in gastric cancer

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

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Gene expression data from myocardial infarction porcine samples

Project description:The use of cDNA microarrays has made it possible to analyze expression of thousands of genes simultaneously. We employed microarray gene expression profiling of porcine cDNA to compare myocardial gene expression in infarct core and remote myocardium at 1 week (n=3), 4 weeks (n=3), and 6 weeks (n=3) after surgically induced myocardial infarction (MI) and in sham-operated controls (n=3). More than 8,000 cDNA sequences were identified in myocardium that showed differential expression in response to MI. Different temporal and spatial patterns of gene expression were recognized in the infarct core tissue within this large set of data. Microarray gene profiling revealed candidate genes, some of them described for the first time, which elucidate changes in biological processes at different stages after MI. We evaluated temporal gene expression in a porcine model of myocardial infarction by microarray technology. Nine female pigs (Sus scrofa crossbreed Landrace x Large White) weighing 30-40 kg were subjected to experimental MI by a double-ligation of the first marginal branch of the circumflex artery. Animals were randomly sacrificed at 1 week (n=3), 4 weeks (n=3), or 6 weeks (n=3) after MI. Three paired myocardial samples from the infarct core and remote myocardium were analyzed at each time point. Myocardial samples from sham-operated animals (open-chest cardiac exposure without coronary artery ligation; n=3) were included as physiological controls.

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