Project description:Intracranial aneurysm is a cerebrovascular disorder in which degeneration of intima and internal elastic lamina of a cerebral artery or vein causes a localized dilation or ballooning of the blood vessel. Different molecular mechanisms are involved in sIA formation in patients. We used microarrays to detail the gene expression of intracranial aneurysm.
Project description:Based on sequencing technology to evaluate the differential lncRNA and mRNA expression of intracranial aneurysms. Provide ideas for the study of epigenetic regulation of intracranial aneurysms
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.
Project description:Intracranial aneurysm (IA) is a pathological dilation of the cerebral artery which has a potential to rupture leading to sub arachnoid haemorrhage (SAH). One third of the patients with aneurysmal SAH (aSAH) develop symptomatic narrowing of the blood vessels called cerebral vasospasm. The outcomes in the above clinical scenarios are variable and devastating. The study was designed to decipher the molecular mechanisms underlying the pathophysiology of intracranial aneurysm formation, its rupture and subsequent development of vasospasm at the proteomic level. The study was done in two phases – discovery phase and validation phase. We performed iTRAQ-based quantitative proteomic analysis of brain vessel tissue and serum samples in three subgroups of patients with IA and compared them with those of control group (subjects with no cerebrovascular disorder) during the discovery phase. In validation phase, dysregulated proteins of biological significance i.e. ORM1 as a biomarker for unruptured aneurysm and MMP9 as a biomarker for cerebral vasospasm were validated in larger cohort of patients.
Project description:Genomic DNA of intracranial aneurysm and matched superficial temporal artery from same patient (n=9) was extracted with QIAamp DNA Mini Kit (Qiagen, Valencia, CA). A total of 500 of genomic DNA was bisulfite conversion using the EZ DNA Methylation Gold Kit (Zymo Research, Irvine, CA) and then analyzed on an Infinium HumanMethylation450 BeadChip (Illumina, San Diego, CA) following the manufacturer’s instructions.
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.
Project description:Comprehensive gene expression profile was obtained by RNA sequencing analysis using total RAN purified from intracranial aneurysm lesions and remaining circle of Willis in rats.
Project description:Recent experimental studies have defined intracranial aneurysms as a macrophage-mediated chronic inflammatory disease affecting intracranial arteries. We used single cell RNA sequencing (scRNA-seq) to analyze the population of macrophages in aneurysm lesions at the growth phase.
Project description:Background and Purpose—Analyzing genes involved in development and rupture of intracranial aneurysms can enhance knowledge about the pathogenesis of aneurysms, and identify new treatment strategies. We compared gene expression between ruptured and unruptured aneurysms and control intracranial arteries. Methods—We determined expression levels with RNA sequencing. Applying a multivariate negative binomial model, we identified genes that were differentially expressed between 44 aneurysms and 16 control arteries, and between 22 ruptured and 21 unruptured aneurysms. The differential expression of 8 relevant and highly significant genes was validated using digital polymerase chain reaction. Pathway analysis was used to identify enriched pathways. We also analyzed genes with an extreme pattern of differential expression: only expressed in 1 condition without any expression in the other. Results—We found 229 differentially expressed genes in aneurysms versus controls and 1489 in ruptured versus unruptured aneurysms. The differential expression of all 8 genes selected for digital polymerase chain reaction validation was confirmed. Extracellular matrix pathways were enriched in aneurysms versus controls, whereas pathways involved in immune response and the lysosome pathway were enriched in ruptured versus unruptured aneurysms. Immunoglobulin genes were expressed in aneurysms, but showed no expression in controls. Conclusions—For rupture of intracranial aneurysms, we identified the lysosome pathway as a new pathway and found further evidence for the role of the immune response. Our results also point toward a role for immunoglobulins in the pathogenesis of aneurysms. Immune-modifying drugs are, therefore, interesting candidate treatment strategies in the prevention of aneurysm development and rupture.