Gene expression profiling of blood in ruptured intracranial aneurysms
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE36791 | GEO | 2014/01/01
SECONDARY ACCESSION(S): PRJNA156747
REPOSITORIES: GEO
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Project description:In the present study we aimed to investigate the systemic response to a rupture of intracranial aneurysms by an analysis of global gene expression profiles in peripheral blood cells. In addition, we sought to determine whether this approach could provide biomarkers related to clinical status of subarachnoid hemorrhage patients. Patients with subarachnoid hemorrhage from ruptured aneurysm were prospectively recruited from patients consecutively admitted to the Departments of Neurology or Neurosurgery and Neurotraumatology, University Hospital, Krakow, Poland in 2010 and 2011. Control subjects were recruited from patients of the Department of Neurology suffered from headaches.
2014-01-01 | E-GEOD-36791 | biostudies-arrayexpress
Project description:The biological mechanisms by which cerebral aneurysms emerge, enlarge and rupture are not totally understood. In the present study, we analyzed the genome-wide gene expression profile in human intracranial aneurysms using cDNA microarrays.
2011-02-01 | GSE26969 | GEO
Project description:The biological mechanisms by which cerebral aneurysms emerge, enlarge and rupture are not totally understood. In the present study, we analyzed the genome-wide gene expression profile in human intracranial aneurysms using cDNA microarrays. Intracranial arterial aneurysm samples (n = 3) and normal superficial temporal artery samples (control, n = 3) were obtained from individual subjects. All aneurysm samples were unruptured aneurysms confirmed by Magnetic Resonance Image or Digital Subtraction Angiography. Affymetrix HU133 Plus 2.0 microarrays were used to compare gene expression levels between aneurismal and normal blood vessels.
2011-02-01 | E-GEOD-26969 | biostudies-arrayexpress
Project description:As the EU IP @neurIST Project aims at integrating biomedical informatics technologies in the assessment of rupture risks and treatments of cerebral aneurysms in humans. Genetic involvement in the disease is known, mRNA biomarkers will be searched as possible risk factors in easy to assess PBMCs (peripheral blood cells). The aim of this pilot study is specifically to check the clinical samples going from the patientï¾s bed side to the genomic analysis platform. Briefly, we hybridized biotin labelled cRNA from 2 controls (C1, C2), 1 patient bearing an intracranial aneurysm (I) and 1 patients bearing an intracranial aneurysm and subarachnoid haemorrhage (S). For each sample, one technical replicate was performed. Thus a total of 8 arrays was used.
2010-12-01 | E-TABM-421 | biostudies-arrayexpress
Project description:Primary multiple intracranial aneurysms (MIA) is a vascular disease that often leads to fatal vascular rupture and subarachnoid hemorrhage. However, little is known about the epigenetic regulation of MIA. Circular RNAs (circRNAs) serve important roles in cardiovascular diseases; however, they have received little research attention regarding their association with MIA. The present study initially aimed to explore novel mechanisms of MIA through circRNA expression profiles. Comprehensive circRNA expression profiles were detected by RNA sequencing (RNA-Seq) in human peripheral blood mononuclear cells. The RNA-Seq results were validated by reverse transcription-quantitative PCR. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses suggested the functions of these circRNAs. Among the 3,328 differentially expressed circRNAs between the MIA and matched groups, 60 exhibited marked expression changes (|log2 fold change|≥2; P<0.05). Among the 60 circRNAs that exhibited significant changes, 20 were upregulated, while the other 40 were downregulated. The circRNAs hsa_circ_0135895, hsa_circ_0000682 and hsa_circ_0000690 could regulate protein tyrosine kinase 2, protein kinase Cβ and integrin subunit αL, respectively. To the best of our knowledge, the present study was the first to perform circRNA sequencing analysis of MIA. Furthermore, the results specifically predicted the regulatory role of circRNAs in MIA pathogenesis.
2020-10-20 | GSE159631 | GEO
Project description:Background and Purpose Aneurysmal subarachnoid hemorrhage, almost always from saccular intracranial aneurysm (sIA), is a devastating form of stroke that affects working age population. Cellular and molecular mechanisms predisposing to the rupture of the sIA wall are largely unknown. Such knowledge would facilitate the design of novel diagnostic tools and therapies for the sIA disease. Methods We compared the whole genome expression profile of eleven ruptured sIA wall samples, resected at a median of 15 hours after rupture, to that of eight unruptured ones. Signaling pathways enriched in the ruptured sIA walls were identified with bioinformatic analyses. Their transcriptional control was predicted in silico by seeking the enrichment of conserved transcription factor binding sites in the promoter regions of differentially expressed genes. Results Overall, 686 genes were significantly upregulated and 740 downregulated in the ruptured sIA walls. Significantly upregulated biological processes included: response to turbulent blood flow; chemotaxis; leukocyte migration; oxidative stress; vascular remodelling; and extracellular matrix degradation. Toll like receptor (TLR) signalling and NF-κB, HIF1A and ETS transcription factor binding sites were significantly enriched among the upregulated genes. Conclusions We identified pathways and candidate genes associated to the rupture of human sIA wall. These results provide a molecular basis analysis (a) to identify rupture-prone sIAs and (b) to prevent their rupture. Novel measures to prevent the rupture of sIA wall may include inhibition of response to turbulent blood flow, leukocyte migration, TLR signalling, or blockade of NF-κB, HIF1A and ETS transcription factors. Human aneurysm pouches were clipped intraoperatively and immediately snap frozen. RNA was extracted from 19 (11 ruptured and 8 unruptured) aneurysm samples and used in microarray hybridization.
2010-12-24 | E-GEOD-13353 | biostudies-arrayexpress
Project description:Gene expression information is useful in prioritizing candidate genes in linkage intervals. The data can also identify pathways involved in the pathophysiology of disease. We used microarrays to identify which genes are expressed in either intracranial arteries (control) or in intracranial aneurysms (case), and can therefore contribute to the disease phenotypes. We used microarrays to identify the pathway membership of expressed genes and the overrepresentation of pathways with expressed genes in the known linkage intervals for intracranial aneurysms. Keywords: Characterization of expression in both diseased and non-diseased intracranial arteries.
2007-11-20 | GSE6551 | GEO
Project description:The rupture of intracranial aneurysm (IA) causes subarachnoid hemorrhage associated with high morbidity and mortality. We compared gene expression profiles in aneurysmal domes between unruptured IAs (UIAs) and ruptured IAs (RIAs) to elucidate biological mechanisms predisposing to the rupture of IA. We determined gene expression levels of eight RIAs, five UIAs, and 10 superficial temporal arteries (STAs) with the Agilent microarrays. To explore biological heterogeneity of IAs, we classified the samples into subgroups showing similar gene expression patterns by using clustering methods. The clustering analysis identified four groups: STAs and UIAs were aggregated their own clusters, whereas RIAs segregated into two distinct subgroups (early and late RIAs). By comparing gene expression levels between early RIAs and UIAs, we identified 430 up-regulated and 617 down-regulated genes in early RIAs. The up-regulated genes were associated with inflammatory and immune responses and phagocytosis including S100/calgranulin genes (S100A8, S100A9, and S100A12). The down-regulated genes suggest mechanical weakness of aneurysm walls. The expressions of Krüppel-like family of transcription factors (KLF2, KLF12, and KLF15), which were anti-inflammatory regulators, and CDKN2A, which was located on chromosome 9p21 that was the most consistently replicated locus in genome-wide association studies of IA, were also down-regulated. We demonstrate that gene expression patterns of RIAs were different according to age of the patients. The results suggest that macrophage-mediated inflammation is a key biological pathway for IA rupture. The identified genes can be good candidates for molecular markers of rupture-prone IAs and therapeutic targets.
2014-07-14 | GSE54083 | GEO
Project description:Background and Purpose Aneurysmal subarachnoid hemorrhage, almost always from saccular intracranial aneurysm (sIA), is a devastating form of stroke that affects working age population. Cellular and molecular mechanisms predisposing to the rupture of the sIA wall are largely unknown. Such knowledge would facilitate the design of novel diagnostic tools and therapies for the sIA disease. Methods We compared the whole genome expression profile of eleven ruptured sIA wall samples, resected at a median of 15 hours after rupture, to that of eight unruptured ones. Signaling pathways enriched in the ruptured sIA walls were identified with bioinformatic analyses. Their transcriptional control was predicted in silico by seeking the enrichment of conserved transcription factor binding sites in the promoter regions of differentially expressed genes. Results Overall, 686 genes were significantly upregulated and 740 downregulated in the ruptured sIA walls. Significantly upregulated biological processes included: response to turbulent blood flow; chemotaxis; leukocyte migration; oxidative stress; vascular remodelling; and extracellular matrix degradation. Toll like receptor (TLR) signalling and NF-κB, HIF1A and ETS transcription factor binding sites were significantly enriched among the upregulated genes. Conclusions We identified pathways and candidate genes associated to the rupture of human sIA wall. These results provide a molecular basis analysis (a) to identify rupture-prone sIAs and (b) to prevent their rupture. Novel measures to prevent the rupture of sIA wall may include inhibition of response to turbulent blood flow, leukocyte migration, TLR signalling, or blockade of NF-κB, HIF1A and ETS transcription factors.
2010-12-24 | GSE13353 | GEO
Project description:The primary aim of the present study was to identify differences on the transcription level between ruptured and unruptured intracranial aneurysms as well as normal intracranial arteries in human. Keywords: Expression profiling by array Global gene expression profiling was performed in human intracranial aneurysms both ruptured (n=8) and unruptured (n=6) as well as in control intracranial arteries (middle meningeal artery, MMA; n=5) using oligonucleotide microarrays.
2010-05-08 | E-GEOD-15629 | biostudies-arrayexpress