Abstract
BackgroundDifferent gene expression profiles are observed in intracranial aneurysm tissue. Understanding these genes and what regulates their expression will help us to understand intracranial aneurysm pathogenesis. We investigated whether differences in gene expression in intracranial aneurysms.MethodsSixteen intracranial aneurysm tissues were compared with 16 matched samples from the superficial temporal artery as controls. We detected the gene expression profiles in these samples with the Human U133 Plus 2.0 GeneChip.ResultsA total of 2142 differentially expressed gene transcripts were detected based on the gene expression profile. Verification analysis showed that the VCAM1, MAGI2, PPP2R2B, PPP2R3A genes were associated with the occurrence and development of intracranial aneurysm. These genes mainly encode cell adhesion molecules (CAMs) and ERK/JNK signaling pathways.ConclusionChanges of genes expression involved in immune and inflammatory reactions, cell adhesion molecules may be associated with the development of aneurysms.
Highlights
Different gene expression profiles are observed in intracranial aneurysm tissue
Genetic factors can lead to changes in hemodynamics, artery structure, inflammation, and autoimmune function, which are linked to the onset of intracranial aneurysms [3–6]
One aneurysm located in right anterior communicating artery (ACoA); three aneurysms located in left internal carotid artery
Summary
Different gene expression profiles are observed in intracranial aneurysm tissue. Understanding these genes and what regulates their expression will help us to understand intracranial aneurysm pathogenesis. We investigated whether differences in gene expression in intracranial aneurysms. Genetic factors remainthe most important indicator for the occurrence, development, and rupture of intracranial aneurysms. Genetic factors can lead to changes in hemodynamics, artery structure, inflammation, and autoimmune function, which are linked to the onset of intracranial aneurysms [3–6]. Many single nucleotide polymorphisms (SNPs) were identified as participating in the formation, development, and rupture of sporadic intracranial aneurysms [7–9]. This study selected the tissue of intracranial aneurysm and superficial temporal artery of the same patients as control group to discuss the mechanism of intracranial aneurysm in gene expression
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