Document Detail


Toll-like receptor 4 expression during cerebral aneurysm formation. Laboratory investigation.
MedLine Citation:
PMID:  19852543     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECT: The pathophysiological origin of cerebral aneurysms is closely associated with chronic inflammation in arterial walls. Recently, the authors identified nuclear factor-kappa B (NF-κB) as a key mediator of cerebral aneurysm formation and progression. Because Toll-like receptor 4 (TLR4) stimulates NF-κB activation in arterial walls in atherosclerosis, the authors hypothesize that TLR4 expresses in cerebral aneurysms and contributes to the activation of NF-κB in cerebral aneurysm walls.
METHODS: Cerebral aneurysms were induced in male Sprague-Dawley rats. Expression of TLRs in cerebral aneurysm walls was assessed using reverse transcriptase polymerase chain reaction (RT-PCR). The expression of TLR4 was examined using RT-PCR, immunohistochemical studies, and Western blotting. To assess TLR4 dependency on NF-κB activation, double immunostaining and a study using NF-κB-deficient mice were done. Finally, TLR4 expression in human cerebral aneurysm walls was assessed using immunohistochemical studies.
RESULTS: In cerebral aneurysm walls, TLR1, -4, -5, -6, -10, and -11 were expressed. Among them, TLR4 and TLR10 expression changed during cerebral aneurysm formation. Expression of TLR4 was predominantly in the endothelial cell layer of cerebral aneurysm walls, and was transitionally upregulated at the early stage of cerebral aneurysm formation. The TLR4 expression coincided well with NF-κB activation. In human cerebral aneurysms, TLR4 was also expressed in the endothelial cell layer, as it was in rats.
CONCLUSIONS: Toll-like receptor 4 was expressed in cerebral aneurysm walls both in rats and humans. This receptor may play a crucial role in cerebral aneurysm formation through NF-κB activation in endothelial cells. The results of the present study will shed new light on the pathogenesis of cerebral aneurysm formation.
Authors:
Tomohiro Aoki; Masaki Nishimura; Ryota Ishibashi; Hiroharu Kataoka; Yasushi Takagi; Nobuo Hashimoto
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neurosurgery     Volume:  113     ISSN:  1933-0693     ISO Abbreviation:  J. Neurosurg.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-04     Completed Date:  2010-10-28     Revised Date:  2013-10-29    
Medline Journal Info:
Nlm Unique ID:  0253357     Medline TA:  J Neurosurg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  851-8     Citation Subset:  AIM; IM    
Affiliation:
Department of Neurosurgery, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western
Humans
Immunohistochemistry
Intracranial Aneurysm / metabolism*,  pathology
Mice
Mice, Knockout
NF-kappa B p50 Subunit / biosynthesis,  genetics
RNA, Messenger / biosynthesis,  isolation & purification
Rats
Rats, Sprague-Dawley
Reverse Transcriptase Polymerase Chain Reaction
Toll-Like Receptor 4 / biosynthesis*
Toll-Like Receptors / biosynthesis
Chemical
Reg. No./Substance:
0/NF-kappa B p50 Subunit; 0/RNA, Messenger; 0/Tlr4 protein, mouse; 0/Toll-Like Receptor 4; 0/Toll-Like Receptors
Comments/Corrections
Erratum In:
J Neurosurg. 2013 Sep;119(3):825-7   [PMID:  23829821 ]

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