Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Intrapericardial administration of secretomes from endometrial-derived mesenchymal stromal cells: effects on immune-related genes in a porcine model of myocardial infarction

ABSTRACT: Using a porcine model of acute myocardial infarction, we explored the potential effect of secretomes from endometrial-derived mesenchymal stromal cells (endMSCs) and from IFNγ/TNFα-primed endMSCs on immune-related genes in the infarcted tissue.

ORGANISM(S): Sus scrofa

PROVIDER: GSE171740 | GEO | 2021/04/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Intrapericardial administration of secretomes from endometrial-derived mesenchymal stromal cells: effects on immune-related genes in a porcine model of myocardial infarction

Project description:Intrapericardial administration of secretomes from endometrial-derived mesenchymal stromal cells: effects on immune-related genes in a porcine model of myocardial infarction

| PRJNA720692 | ENA

Intrapericardial Administration of Secretomes from Menstrual Blood-Derived Mesenchymal Stromal Cells: Effects on Immune-Related Genes in a Porcine Model of Myocardial Infarction.

Project description:Acute myocardial infarction (AMI) is a manifestation of ischemic heart disease where the immune system plays an important role in the re-establishment of homeostasis. We hypothesize that the anti-inflammatory activity of secretomes from menstrual blood-derived mesenchymal stromal cells (S-MenSCs) and IFNγ/TNFα-primed MenSCs (S-MenSCs*) may be considered a therapeutic option for the treatment of AMI. To assess this hypothesis, we have evaluated the effect of S-MenSCs and S-MenSCs* on cardiac function parameters and the involvement of immune-related genes using a porcine model of AMI. Twelve pigs were randomly divided into three biogroups: AMI/Placebo, AMI/S-MenSCs, and AMI/S-MenSCs*. AMI models were generated using a closed chest coronary occlusion-reperfusion procedure and, after 72 h, the different treatments were intrapericardially administered. Cardiac function parameters were monitored by magnetic resonance imaging before and 7 days post-therapy. Transcriptomic analyses in the infarcted tissue identified 571 transcripts associated with the Gene Ontology term Immune response, of which 57 were differentially expressed when different biogroups were compared. Moreover, a prediction of the interactions between differentially expressed genes (DEGs) and miRNAs from secretomes revealed that some DEGs in the infarction area, such as STAT3, IGFR1, or BCL6 could be targeted by previously identified miRNAs in secretomes from MenSCs. In conclusion, the intrapericardial administration of secretome early after infarction has a significant impact on the expression of immune-related genes in the infarcted myocardium. This confirms the immunomodulatory potential of intrapericardially delivered secretomes and opens new therapeutic perspectives in myocardial infarction treatment.

| S-EPMC9138214 | biostudies-literature

Mouse model of myocardial infarction

Project description:This dataset is a time series (1 hour [h], 4 hours, 24 hours, 48 hours, 1 week [w], and 8 weeks) intended to compare normal functioning left ventricles [lv + lv2] with infarcted [ilv] and non-infarcted left ventricles [nilv]. Ilv samples are taken from the region between the LAD artery and the apex on a mouse with myocardial infarction. Lv2 samples are from the same region in a sham operated mouse. Nilv samples are taken from the region above the infartion and the left ventricle [lv] samples mimic that region in a sham mouse. The lv and lv2 samples can be compared as both are from normal functioning hearts. For more information visit http://cardiogenomics.med.harvard.edu/groups/proj1/pages/mi_home.html Keywords: other

2003-10-24 | GSE775 | GEO

ATP2A2 and miRNA in human myocardial infarction

Project description:Cardiac sarco(endo)plasmic reticulum calcium ATPase-2 (SERCA2) plays one of the central roles in myocardial contractility. Both, SERCA2 mRNA and protein are reduced in myocardial infarction (MI), but the correlation has not been always observed. MicroRNAs (miRNAs) act by targeting 3'-UTR mRNA, causing translational repression in physiological and pathological conditions, including cardiovascular diseases. The aim of our study was to identify miRNAs that could influence SERCA2 expression in human MI. The protein SERCA2 was decreased and 43 miRNAs were deregulated in infarcted myocardium compared to remote myocardium. miRNAs binding prediction to SERCA2 identified 213 putative miRNAs. TAM and miRNApath identified 18 functional and 21 diseased states related to heart diseases. Combing all results, we identified certain miRNAs as potential regulators of SERCA2. All the samples were stored as FFPE tissue and in RNAlater. Expression of SERCA2 was analyzed by western blot and miRNA expression was analyzed by microarrays and qPCR in samples of remote and infarcted myocardium from 6 patients who died of MI. Bioinformatic analysis including six prediction programmes (TargetScan, PicTar, miRBase, miRDB, Human MicroRNA Targets, and microrna.org), TAM and miRNApath annotation, and free-energy of binding (RNA22, RNAfold), was performed. Nine up-regulated miRNAs were analyzed for free-energy of binding and flanking regions, and nine miRNAs were used for validation with qPCR. Based on qPCR the comparison between FFPE and RNAlater as well as different reference genes was also performed.

2012-04-29 | E-GEOD-17304 | biostudies-arrayexpress

Effect of therapy-induced secretomes on the transcriptome of ovarian cancer cells

Project description:Exogenous signals from drug-stressed cancer cells promote acquisition of a more aggressive phenotype of neighboring tumor cells. Recently, we examined how cancer cell secretome changes in response to chemotherapy. We showed that tumor therapy-induced secretomes significantly increased resistance of cancer cells to subsequent cisplatin treatment but we did not observed the same phenomenon on normal fibroblasts. To elucidate how therapy-induced secretomes affect the transcriptomic profiles of recipient tumor cells, we incubated SKOV3 cells for 3 days with secretomes from control or dying cancer cells. The same conditions were used for normal fibroblasts. Enrichment analysis of differentially expressed genes in SKOV3 cells incubated with therapy-induced secretomes identified prominent up-regulation of genes involved in coordination of mitotic processes, G2/M transition checkpoints and DNA repair. These findings demonstrate that under stress condition cancer but not normal cells can secrete signaling molecules into the exracellular space and contribute to the emergence of tumor chemoresistance during short time period.

2024-04-24 | GSE241910 | GEO

Regulation of gene expression with thyorid hormone in rats with myocardial infarction

Project description:Thyroid hormone improves left ventricular remodeling and cardiac performance after myocardial infarction (MI), but the molecular basis is unknown. This study was designed to detect gene expression changes in left ventricular non-infarcted areas at 4 weeks following myocardial infarction with and without thyroid hormone treatment. The results suggest that altered expression of genes for molecular function and biological process may be involved in the beneficial effects of thyroid hormone treatment following myocardial infarction in rats. MI was produced by ligation of the left anterior descending coronary artery in female SD rats. Rats were divided into the following groups: (1) Sham MI, (2) MI, and (3) MI+T4 treatment (T4 pellet 3.3mg, 60 days release, implanted subcutaneously immediately following MI). Four weeks after surgery, total RNA was isolated from left ventricular non-infarcted areas for microarray analysis using the Illumina RatRef-12 Expression BeadChip Platform.

2012-04-30 | E-GEOD-35088 | biostudies-arrayexpress

Gasdermin D inhibition confers antineutrophil mediated cardioprotection in acute myocardial infarction

Project description:Acute myocardial infarction (AMI) induces blood leukocytosis, which correlates inversely with patient survival. The molecular mechanisms leading to leukocytosis, and recruitment to the infarcted heart, remain poorly understood. Using an AMI mouse model, gasdermin D (GSDMD) was identified in activated neutrophils early in AMI. We demonstrated that GSDMD is required for enhanced recruitment of neutrophils and monocytes to the infarcted heart. Loss of GSDMD resulted in reduced release of IL-1β from neutrophils and reduced recruitment of neutrophils and monocytes to the infarcted heart. Knockout of GSDMD in mice significantly reduced infarct size, improved cardiac function and increased survival post AMI. Through a series of bone marrow transplantation studies and leukocytes depletion experiments, we further demonstrated that excessive bone marrow derived and GSDMD-dependent neutrophil recruitment, contributes to the detrimental immunopathology after AMI. Pharmacological inhibition of GSDMD also conferred cardioprotection post AMI, through reduction of scar size and enhancement of heart function. Our study provides new mechanistic insights into molecular regulation of neutrophil generation and recruitment after AMI, and supports GSDMD as a new target for improved ventricular remodeling and reduced heart failure after AMI.

2022-01-05 | GSE181872 | GEO

CCN3 administration after surgically induced myocardial infarction

Project description:CCN3 administration after surgically induced myocardial infarction

2023-02-27 | GSE217925 | GEO

RNA sequencing analysis of mouse cardiac endothelial cells in myocardial infarction tissues

Project description:To investigate the transcriotome alteration in endothelial cells (ECs) under a myocardial infarction (MI) condition, we performed RNA sequcening analysis with sorted ECs derived from mouse infarcted cardiac tissues or normal left ventricle (LV).

2021-12-31 | GSE163772 | GEO

MiR-155 promotes blood-brain barrier dysfunction in neuroinflammation (part 1)

Project description:Here, we investigated the time-course changes in the pattern of microRNA (miRNA) expression of TNFα and IFNγ-stimulated and unstimulated hCMEC/D3 cells, an immortalized human cerebral microvascular endothelial cell line. In order to investigate pro-inflammatory cytokine-induced changes in miRNA levels in hCMEC/D3 cells, we challenged brain endothelial cells with TNFα and IFNγ (100 ng/ml) for 2 h, 6 h and 24 h and determined microRNA expression in cytokine-stimulated and unstimulated cells

2014-04-29 | E-GEOD-44692 | biostudies-arrayexpress