Gene expression data from myocardial infarction porcine samples
Ontology highlight
ABSTRACT:
ORGANISM(S): Sus scrofa
PROVIDER: GSE34569 | GEO | 2013/03/01
SECONDARY ACCESSION(S): PRJNA151011
REPOSITORIES: GEO
Similar Datasets
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.
2013-03-01 | E-GEOD-34569 | biostudies-arrayexpress
Project description:The Murphy Roth Large (MRL) mouse, a strain capable of regenerating right ventricular myocardium, has a high post-myocardial infarction (MI) survival rate compared with C57BL6/J (C57) mice. The biological processes responsible for this survival advantage are unknown. We compared acute post-MI gene expression in C57 and MRL hearts using microarrays and identified promising candidate biological processes underlying increased survival in the MRL. Hearts from both strains were excised at different time points before or after MI for RNA extraction and hybridization to MOE430A arrays. Baseline hearts were excised from healthy mice that had not undergone the MI procedure (day 0). Infarct tissue in this case means tissue taken from the anterior-apical region that would be the infarct region in a post-MI heart. Non-infarct covers the remainder of the LV. Post-MI hearts were excised either 1 or 5 days after MI. We had successful hybridizations for 3 replicates each of C57 day 0 infarct and non-infarct tissue (6 arrays), 4 MRL day 0 infarct and non-infarct tissue (8 arrays), 4 C57 day 1 infarct and non-infarct tissue (8 arrays), 4 MRL day 1 infarct and non-infarct tissue (8 arrays), 4 C57 day 5 infarct and non-infarct tissue (8 arrays), and 4 MRL day 5 infarct and non-infarct tissue (8 arrays).
2010-05-27 | E-GEOD-19322 | biostudies-arrayexpress
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
Project description:Background. Accumulation of extracellular matrix in the myocardium attenuates cardiac contractile function, and predisposes to arrhythmias and sudden cardiac death. Connective tissue growth factor (CTGF) is a matricellular protein that has been shown to promote development of cardiac fibrosis. Objectives. To investigate for the potential of CTGF monoclonal antibody (CTGF mAb) in protecting from development of cardiac fibrosis following myocardial infarction (MI), and to evaluate its effect during infarct repair and acute cardiac ischemia-reperfusion (I/R) injury. Methods. Mice were subjected to MI or to I/R injury and treated with either control IgG or CTGF mAb. Cultured human cardiac fibroblasts were used to investigate the signalling mechanisms modulated by CTGF mAb. Results. Treatment with CTGF mAb for four days from day three after MI improved survival, attenuated infarct expansion, and resulted in better preserved left ventricular (LV) systolic function. CTGF mAb therapy for six weeks from day seven after MI reduced the MI-induced increase in cardiomyocyte size, heart weight to body weight ratio and remote LV fibrosis. RNA sequencing analysis of LV samples showed that CTGF mAb induced expression of cardiac repair/developmental genes and normalized the MI-induced increase in expression of inflammatory/profibrotic genes. CTGF mAb induced c-Jun N-terminal kinase (JNK) phosphorylation in vivo and in vitro, and inhibition of JNK abrogated the reduced collagen production in CTGF mAb treated fibroblasts. Conclusions. Treatment with CTGF mAb induces expression of cardiac repair/developmental genes and inhibits expression of inflammatory/pro-fibrotic genes in MI hearts providing benefit during post-MI cardiac repair and reducing post-MI cardiac fibrosis.
2019-04-02 | GSE129134 | GEO
Project description:Closed-chest reperfused MI was induced in pigs by 90-min occlusion, followed by reperfusion of the mid LAD (day 0) and by cardiac MRI with late enhancement (LE) at day 3. At day 30 the animals received either porcine APOSEC (n=8) or placebo medium (n=8) in a randomized manner, injected into the border zone of MI using 3D NOGA percutaneous intramyocardial guidance. At day 60, control cardiac MRI with LE and measurements of myocardial viability via diagnostic NOGA were performed. Gene expression profiling of the infarct core, border zone and normal myocardium was performed using microarray analysis, confirmed by quantitative real-time PCR. Percutaneous endomyocardial injections of APOSEC led to a significant (p<0.05) decrease in infarct size and in improvement of cardiac index and myocardial viability compared to medium treatment. Trend towards higher LV ejection fraction was observed in APOSEC vs. the Medium placebo group (45.4M-BM-15.9% vs 37.4M-BM-18.9%, p=0.052). Transcriptome analysis revealed significant downregulation of caspase-1 and other inflammatory genes in the APOSEC-affected areas. PCR showed higher expression of myogenic factor, Mefc2 (p<0.05) gene with downregulated caspase-3 (p<0.05) in the APOSEC-pigs. We have investigated the effects of catheter-based endomyocardial injections of APOSEC (secretome of apoptotic peripheral white blood cells) on porcine chronic post-infarction (MI) left ventricular (LV) dysfunction and gene expression profile. Pigs randomized to receive eithersecretome (n=8) or medium (placebo control, n=8)
2013-12-31 | E-GEOD-47397 | biostudies-arrayexpress
Project description:Myocardial infarction (MI) results from occlusion of blood supply to the heart muscle causing death of cardiac muscle cells. Following myocardial infarction (MI), scar formation acts to mechanically stabilise the injured heart to prevent rupture and death. While fibroblasts and macrophages are implicated in post-MI scar formation and maturation, their exact contributions to this process are poorly characterised, especially in the long-term (i.e., beyond 1-week post-MI). Here, we employ state-of-the-art spatially-targetted optical micro-proteomics (STOMP) to isolate proteomes of tissue fractions enriched for fibroblasts (sma+) and macrophages (cd68+) over a 6-week post-MI timecourse and compare them to whole-scar proteome. We illustrate dynamic, specific changes in sma- and cd68-enriched fraction protein composition over 1-6 weeks post-MI with some of these changes reflected in whole-infarct preparations. These results link specific cell populations to specific protein changes in whole infarct.
2023-10-31 | PXD034413 | Pride
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.
2014-05-26 | E-GEOD-54612 | biostudies-arrayexpress
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.
2012-04-30 | GSE17304 | GEO
Project description:Neuregulin-1 (NRG-1) is a paracrine factor critical for cardiac development. We have been examining whether the recombinant NRG-1β isoform known as glial growth factor 2 (GGF2) has therapeutic potential for heart failure. In both small and large animals after experimental myocardial infarction (MI) we have found that GGF2 treatment improves myocardial function and limits progressive myocardial remodeling. To understand potential mechanisms for this effect, we compared gene expression in swine by microarray analysis. We used microarrays to compared th the global gene expression underlying the efficacy of GGF2 treatment for heart injury. Left ventricular tissue remote from the site of infarct was collected from each of 8 animals (3 untreated controls, 3 low dose GGF2-treated and 2 high dose GGF2-treated) and processed for gene expression microarray analysis using Affymetrix porcine genome GeneChips.
2014-06-21 | E-GEOD-48255 | biostudies-arrayexpress
Project description:Closed-chest reperfused MI was induced in pigs by 90-min occlusion, followed by reperfusion of the mid LAD (day 0) and by cardiac MRI with late enhancement (LE) at day 3. At day 30 the animals received either porcine APOSEC (n=8) or placebo medium (n=8) in a randomized manner, injected into the border zone of MI using 3D NOGA percutaneous intramyocardial guidance. At day 60, control cardiac MRI with LE and measurements of myocardial viability via diagnostic NOGA were performed. Gene expression profiling of the infarct core, border zone and normal myocardium was performed using microarray analysis, confirmed by quantitative real-time PCR. Percutaneous endomyocardial injections of APOSEC led to a significant (p<0.05) decrease in infarct size and in improvement of cardiac index and myocardial viability compared to medium treatment. Trend towards higher LV ejection fraction was observed in APOSEC vs. the Medium placebo group (45.4±5.9% vs 37.4±8.9%, p=0.052). Transcriptome analysis revealed significant downregulation of caspase-1 and other inflammatory genes in the APOSEC-affected areas. PCR showed higher expression of myogenic factor, Mefc2 (p<0.05) gene with downregulated caspase-3 (p<0.05) in the APOSEC-pigs. We have investigated the effects of catheter-based endomyocardial injections of APOSEC (secretome of apoptotic peripheral white blood cells) on porcine chronic post-infarction (MI) left ventricular (LV) dysfunction and gene expression profile.
2013-12-31 | GSE47397 | GEO