Document Detail

Molecular anatomy of an intracranial aneurysm: coordinated expression of genes involved in wound healing and tissue remodeling.
MedLine Citation:
PMID:  11283408     Owner:  NLM     Status:  MEDLINE    
BACKGROUND AND PURPOSE: Approximately 6% of human beings harbor an unruptured intracranial aneurysm. Each year in the United States, >30 000 people suffer a ruptured intracranial aneurysm, resulting in subarachnoid hemorrhage. Despite the high incidence and catastrophic consequences of a ruptured intracranial aneurysm and the fact that there is considerable evidence that predisposition to intracranial aneurysm has a strong genetic component, very little is understood with regard to the pathology and pathogenesis of this disease. METHODS: To begin characterizing the molecular pathology of intracranial aneurysm, we used a global gene expression analysis approach (SAGE-Lite) in combination with a novel data-mining approach to perform a high-resolution transcript analysis of a single intracranial aneurysm, obtained from a 3-year-old girl. RESULTS: SAGE-Lite provides a detailed molecular snapshot of a single intracranial aneurysm. These data suggest that, at least in this specific case, aneurysmal dilation results in a highly dynamic cellular environment in which extensive wound healing and tissue/extracellular matrix remodeling are taking place. Specifically, we observed significant overexpression of genes encoding extracellular matrix components (eg, COL3A1, COL1A1, COL1A2, COL6A1, COL6A2, elastin) and genes involved in extracellular matrix turnover (TIMP-3, OSF-2), cell adhesion and antiadhesion (SPARC, hevin), cytokinesis (PNUTL2), and cell migration (tetraspanin-5). CONCLUSIONS: Although these are preliminary data, representing analysis of only one individual, we present a unique first insight into the molecular basis of aneurysmal disease and define numerous candidate markers for future biochemical, physiological, and genetic studies of intracranial aneurysm. Products of these genes will be the focus of future studies in wider sample sets.
D G Peters; A B Kassam; E Feingold; E Heidrich-O'Hare; H Yonas; R E Ferrell; A Brufsky
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Publication Detail:
Type:  Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Stroke; a journal of cerebral circulation     Volume:  32     ISSN:  1524-4628     ISO Abbreviation:  Stroke     Publication Date:  2001 Apr 
Date Detail:
Created Date:  2001-04-03     Completed Date:  2001-04-26     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0235266     Medline TA:  Stroke     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1036-42     Citation Subset:  IM    
Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, PA, USA.
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MeSH Terms
Calcium-Binding Proteins / genetics,  metabolism
Cell Adhesion Molecules / genetics,  metabolism
Cell Cycle Proteins / genetics,  metabolism
Cerebral Angiography
Child, Preschool
Expressed Sequence Tags
Extracellular Matrix Proteins / genetics,  metabolism
Gene Expression*
Gene Expression Profiling / methods
Gene Frequency
Glycoproteins / genetics,  metabolism
Inflammation / pathology
Intracranial Aneurysm / genetics*,  metabolism,  pathology
Membrane Proteins / genetics,  metabolism
Middle Cerebral Artery / metabolism,  pathology*
Osteonectin / genetics,  metabolism
RNA, Messenger / metabolism
Regeneration / genetics*
Tissue Inhibitor of Metalloproteinase-3 / genetics,  metabolism
Wound Healing / genetics*
Grant Support
Reg. No./Substance:
0/Calcium-Binding Proteins; 0/Cell Adhesion Molecules; 0/Cell Cycle Proteins; 0/Extracellular Matrix Proteins; 0/Glycoproteins; 0/Membrane Proteins; 0/Osteonectin; 0/POSTN protein, human; 0/RNA, Messenger; 0/SPARCL1 protein, human; 0/Sparcl1 protein, mouse; 0/Tissue Inhibitor of Metalloproteinase-3
Comment In:
Stroke. 2001 Nov;32(11):2725-6   [PMID:  11692046 ]

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