MicroRNA and gene expression changes in human cerebral aneurysms [expression array]
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ABSTRACT:
ORGANISM(S): synthetic construct Homo sapiens
PROVIDER: GSE66239 | GEO | 2016/02/24
SECONDARY ACCESSION(S): PRJNA276505
REPOSITORIES: GEO
Similar Datasets
Project description:Cerebral Aneurysm tissues and superficial temporal arteries were compared through RNA-Seq to identify differentially expressed genes, and through microRNA microarray to identify differentially expressed microRNAs. Significant miR:gene pairs were identified for potential microRNA silencing regualtory effects.
2016-02-24 | GSE66238 | GEO
Project description:Cerebral Aneurysm tissues and superficial temporal arteries were compared through RNA-Seq to identify differentially expressed genes, and through microRNA microarray to identify differentially expressed microRNAs. Significant miR:gene pairs were identified for potential microRNA silencing regualtory effects. To study differentially expressed genes and microRNAs in cerebral aneurysms, we collected 7 cerebral aneurysm tisses and 10 superficial temporal artery (STA) tisses from 17 individuals. We performed RNA-Seq and microRNA microarray analysis on these samples, and compared them using STA as a control.
2016-02-24 | E-GEOD-66238 | 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. 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: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: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: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:In this study we used microarrays to examine relative genes expression within the aorta of ApoE-/- infused with angiotensin II in relation to aneurysm formation. Infusion of angiotensin II induces aortic dilatation particularly of the suprarenal aorta in ApoE-/- mice. Based on studies carried out in our and other laboratories the response to angiotensin II is variable, with some mice developing large aneurysms but other animals appearing resistant to aneurysm formation with aortic diameters similar to that of saline controls. We compared RNA expression from whole aortas of 17 week old male ApoE-/- mice exposed to angiotensin II (1.44 µg/kg/min) for 4 weeks where there was clear evidence of aortic aneurysm formation (n=5) with that of mice failing to develop aneurysms (n=7) and those exposed to saline infusion (n=6). AAA was defined as diameter of suprarenal aorta greated than 1.5mm measured on photographs of aortas at necroscopy. Keywords: Disease state analysis 18 samples analysed, AAA (n=5), no AAA (n=7), saline (n=6). AAA - abdominal aortic aneurysm
2010-06-24 | E-GEOD-12591 | biostudies-arrayexpress
Project description:Arraystar Human circRNA Microarray is designed for the profiling of human circRNAs. In this study, we applied a circRNA microarray to screen the potential biomarker for intracranial aneurysm. A total of 10 samples were used to perform microarray analysis. Our study contained 2 groups, un-ruptured intracranial aneurysm group(B1-B5) and ruptured intracranial aneurysm group(C1-C5). Each group contained five samples.
2021-07-15 | E-MTAB-10683 | biostudies-arrayexpress
Project description:Smooth muscle cell TGFβ signaling is one of the primary drivers of smooth muscle cell maturation. Inhibition of smooth muscle cell TGFβ signaling in hyperlipidemic mice induces vessel wall inflammation and vessel wall dilation/dissection and leads aortic aneurysm. We performed bulk RNAseq method to examine smooth muscle cell gene expression profile using fresh human tissues from normal aortic media smooth muscle cells and aneurysm aortic media smooth muscle cells.
2020-03-01 | GSE140947 | GEO
Project description:We report on the early pathological development of a well-established murine model of aortic dissection / abdominal aortic aneurysm.
2018-12-15 | GSE123874 | GEO