Gene Expression Following Cardioembolic Stroke
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE58294 | GEO | 2014/09/02
SECONDARY ACCESSION(S): PRJNA251940
REPOSITORIES: GEO
Similar Datasets
Project description:Blood from subjects with cardioembolic stroke and controls was collected, and the RNA extracted was interrogated and whole genome U133 Affymetrix Arrays. Twenty-three control samples and sixty-nine cardioembolic stroke samples were assayed. Blood from subjects with cardioembolic stroke and controls was collected, and the RNA extracted was interrogated and whole genome U133 Affymetrix Arrays. Twenty-three control samples and sixty-nine cardioembolic stroke samples were assayed. Cardioembolic stroke subjects were analyzed at three time points: less than 3 hours, 5 hours, and 24 hours following the event.
2014-09-02 | E-GEOD-58294 | biostudies-arrayexpress
Project description:The purpose of this project was to elucidate gene expression in the peripheral whole blood of acute ischemic stroke patients to identify a panel of genes for the diagnosis of acute ischemic stroke. Peripheral blood samples were collected in Paxgene Blood RNA tubes from stroke patients who were >18 years of age with MRI diagnosed ischemic stroke and controls who were non-stroke neurologically healthy. The results suggest a panel of genes can be used to diagnose ischemic stroke, and provide information about the biological pathways involved in the response to acute ischemic stroke in humans. Total RNA extracted from whole blood in n=39 ischemic stroke patients compared to n=24 healthy control subjects.
2010-06-08 | E-GEOD-16561 | biostudies-arrayexpress
Project description:Background and Purpose The neurological course after stroke is highly variable and is determined by demographic, clinical, and genetic factors. However, other heritable factors such as epigenetic DNA methylation could play a role in neurological changes after stroke. Methods We performed a three-stage epigenome-wide association study (EWAS) to evaluate DNA methylation associated with the difference between the National Institutes of Health Stroke Scale (NIHSS) at baseline and at discharge (ΔNIHSS) in ischemic stroke patients. DNA methylation data in the Discovery (n = 643) and Replication (n = 62) Cohorts were interrogated with the 450K and EPIC BeadChip. Nominal CpG-sites from the Discovery (p-value < 10-06) were also evaluated in a meta-analysis of the Discovery and Replication cohorts, using a random-fixed effect model. Specific cell type methylation was assessed using EpiDISH. We integrated the methylation data with 1305 plasma protein expression levels measured by SOMAscan and measured RNA expression with RT-PCR in a subgroup of 13 subjects. Results The meta-analysis revealed an epigenome-wide significant association in EXOC4 (p-value = 8.4x10-08) and in MERTK (p-value = 1.56x10-07). Only the methylation in EXOC4 was also associated in the Discovery and in the Replication cohort (p-value = 1.14x10-06 and p-value = 1.3x10-02, respectively). EXOC4 methylation negatively correlated with the long-term outcome (coefficient = -5.89) and showed a tendency towards a decrease in EXOC4 expression (rho = -0.469, p-value = 0.091). Pathway enrichment from the meta-analysis revealed significant associations related with the exocytic process. Seventy-nine plasma proteins were differentially expressed in association with EXOC4 methylation. Pathway analysis of these proteins showed an enrichment in Natural Killer cell activation. Conclusions DNA methylation of EXOC4 is associated with a worse neurological course after stroke. Pathway analysis suggests that the exocytic pathway could be a potential biological mechanism underlying this association. Background and Purpose The neurological course after stroke is highly variable and is determined by demographic, clinical, and genetic factors. However, other heritable factors such as epigenetic DNA methylation could play a role in neurological changes after stroke. Methods We performed a three-stage epigenome-wide association study (EWAS) to evaluate DNA methylation associated with the difference between the National Institutes of Health Stroke Scale (NIHSS) at baseline and at discharge (ΔNIHSS) in ischemic stroke patients. DNA methylation data in the Discovery (n = 643) and Replication (n = 62) Cohorts were interrogated with the 450K and EPIC BeadChip. Nominal CpG-sites from the Discovery (p-value < 10-06) were also evaluated in a meta-analysis of the Discovery and Replication cohorts, using a random-fixed effect model. Specific cell type methylation was assessed using EpiDISH. We integrated the methylation data with 1305 plasma protein expression levels measured by SOMAscan and measured RNA expression with RT-PCR in a subgroup of 13 subjects. Results The meta-analysis revealed an epigenome-wide significant association in EXOC4 (p-value = 8.4x10-08) and in MERTK (p-value = 1.56x10-07). Only the methylation in EXOC4 was also associated in the Discovery and in the Replication cohort (p-value = 1.14x10-06 and p-value = 1.3x10-02, respectively). EXOC4 methylation negatively correlated with the long-term outcome (coefficient = -5.89) and showed a tendency towards a decrease in EXOC4 expression (rho = -0.469, p-value = 0.091). Pathway enrichment from the meta-analysis revealed significant associations related with the exocytic process. Seventy-nine plasma proteins were differentially expressed in association with EXOC4 methylation. Pathway analysis of these proteins showed an enrichment in Natural Killer cell activation. Conclusions DNA methylation of EXOC4 is associated with a worse neurological course after stroke. Pathway analysis suggests that the exocytic pathway could be a potential biological mechanism underlying this association.
2022-05-20 | GSE203399 | GEO
Project description:Genetic differences in endothelial biology could underlie development of phenotypic heterogeneity amongst individuals afflicted with vascular diseases. We obtained BOEC (blood outgrowth endothelial cells) from 20 subjects with sickle cell anemia (age 4-19) shown to be either at-risk (n=11) or not-at-risk (n=9) for ischemic stroke due to, respectively, having or not having occlusive disease at the Circle of Willis (CoW). Gene expression profiling identified no significant single gene differences between the two groups, as expected. However, analysis of Biological Systems Scores, using gene sets that were pre-determined to survey each of nine biological systems, showed that only changes in inflammation signaling are characteristic of the at-risk subjects, as supported by multiple statistical approaches Keywords: disease status analysis
2007-12-18 | GSE9877 | GEO
Project description:Genetic differences in endothelial biology could underlie development of phenotypic heterogeneity amongst individuals afflicted with vascular diseases. We obtained BOEC (blood outgrowth endothelial cells) from 20 subjects with sickle cell anemia (age 4-19) shown to be either at-risk (n=11) or not-at-risk (n=9) for ischemic stroke due to, respectively, having or not having occlusive disease at the Circle of Willis (CoW). Gene expression profiling identified no significant single gene differences between the two groups, as expected. However, analysis of Biological Systems Scores, using gene sets that were pre-determined to survey each of nine biological systems, showed that only changes in inflammation signaling are characteristic of the at-risk subjects, as supported by multiple statistical approaches Experiment Overall Design: We obtained BOEC (blood outgrowth endothelial cells) from 20 subjects with sickle cell anemia (age 4-19) shown to be either at-risk (n=11) or not-at-risk (n=9) for ischemic stroke due to, respectively, having or not having occlusive disease at the Circle of Willis (CoW). To allow power calculations to be done, we performed microarray analysis on BOEC from 27 normal subjects of diverse ages. Gene expression profilings were obtained by using Affymetrix U133A chips
2008-06-17 | E-GEOD-9877 | biostudies-arrayexpress
Project description:To evaluate lncRNA expression and changes in whole blood samples of patients during the acute cerebral ischemia phase, we have employed whole genome microarray expression profiling as a discovery platform to identify dysregulated genes to put forth predicted connections and functions of the differentially expressed lncRNAs.There were 1123 differentially expressed lncRNAs (Fold change ≥2.0, p<0.05) between stroke patients and the control group. Among these, 371 lncRNAs were upregulated, and 752 lncRNAs were downregulated. Expression of nine lncRNAs (ENST00000452599, ENST00000527450, ENST00000608826, T013651, T029143, T131416, T294865, ENST00000530525 and T058035) from this signature was quantified in the same RNA samples by real-time PCR, confirming our gene chip performance.
2022-03-20 | GSE198710 | GEO
Project description:Atrial fibrillation (AF) is a major risk factor for cardioembolic stroke. Anticoagulant drugs are effective in preventing AF-related stroke. However, the high frequency of anticoagulant-associated major bleeding is a major concern particularly when antiplatelet treatment is simultaneously administered. Here, microarray analysis in peripheral blood cells in eight patients with AF and stroke and eight AF subjects without stroke identified a stroke related gene expression pattern. HSPA1B, which encodes for heat-shock protein 70 kDa (Hsp70), was the most differentially expressed gene. This gene was downregulated in stroke subjects, a finding confirmed further in an independent AF cohort of 200 individuals. Hsp70 knock-out (KO) mice subjected to different thrombotic challenges developed thrombosis significantly earlier than their wild-type (WT) counterparts. In WT mice, Hsp70 inducers (TRC051384, or tubastatin A) delayed thrombus formation. Remarkably, Hsp70 inducers did not increase the bleeding risk even when aspirin was concomitantly administered. Hsp70 induction was associated with an increased vascular thrombomodulin expression, higher circulating levels of activated protein C (APC) upon thrombotic stimulus and increased protection against endothelial apoptosis. Thus, Hsp70 induction is a novel approach to delay thrombus formation with minimal bleeding risk, being especially promising in situations where there is a major bleeding hazard. Microarray analysis in peripheral blood cells includes eight patients with AF and stroke and eight AF subjects without stroke
2016-04-01 | E-GEOD-66724 | biostudies-arrayexpress
Project description:Sixty-nine samples obtained from surgical excision with overall survival.
| PRJNA296897 | ENA
Project description:To discover biomarkers for stroke, untargeted LC/MS-based metabolomics was performed in 42 plasma samples from subjects of prognosis and non-prognosis. The results showed that there were 10 up-regulated markers and 26 down-regulated markers.
2022-06-27 | MSV000089746 | MassIVE
Project description:Purpose: Signaling pathways mediated by microRNAs (miRNAs) represent one of the mechanisms that regulate stroke progression and recovery. The goal of this study is to investigate miRNA expression signatures in freshly removed human stroke brain tissue. Methods: Human brain samples (5 stroke and 3 non-stroke samples) obtained at 48-72 hours after stroke onset during craniectomy and stroke-ectomy, were subjected to histopathological and immunofluorescence microscopy analyses. NGS sequencing was performed by Qiagen company and analyses were carried out using QIAseq miRNA Quantification workflow and RNA-seq Analysis tools within CLC Genomics Workbench (version 20.0.2). Reads were normalized for expression analysis using trimmed mean of M-values method (TMM). miRNA profiling was performed using the EdgeR in Bioconductor package. Whole transcriptome RNA-sequencing Analysis: The unmapped reads from the NGS miRNA analysis were extracted, deduplicated and mapped to the genome. Gene expressions were calculated by counting number of reads mapping to the annotated gene loci. Human miR-155 Targets RT2 Profiler PCR Array (Qiagen) was performed using 3 RNA samples per stroke and control groups. The PCR Array Data analysis was performed using an automated PCR Analysis Web Portal and GeneGlobe Data Analysis (Qiagen). Results: Human stroke brain tissue was characterized by classic ischemic changes, including significant neuronal and vascular damage, and prominent edema. The absence of monocytes and notable neutrophil infiltration indicated the early stage of leukocyte response to ischemia. miRNA NGS analysis detected 36 miRNAs with significantly aberrant expression in stroke tissue, as compared to non-stroke samples. Of these miRNAs, 19 were previously identified in stroke patient blood and CSF, while dysregulation of 16 miRNAs was newly detected in this study. Bioinformatics pathway enrichment analysis demonstrated a strong association of the identified miRNAs with stroke-related biological processes and signaling pathways Conclusions: Dysregulated miRNAs detected in our study could be regarded as potential candidates for biomarkers and/or targets for therapeutic intervention. The obtained data will serve for better understanding of the molecular basis of stroke and provide valuable information for the future functional studies in the experimental models of stroke.
2020-07-29 | GSE155257 | GEO