Document Detail

Inflammatory responses involving tumor necrosis factor receptor-associated factor 6 contribute to in-stent lesion formation in a stent implantation model of rabbit carotid artery.
MedLine Citation:
PMID:  16520179     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Inflammatory responses are considered to represent a unique property after stent implantation, and we previously demonstrated that inflammatory signaling involving tumor necrosis factor receptor-associated factor 6 (TRAF6) contributes to neointimal formation in a balloon injury model of rabbit carotid artery. The purpose of this study was to examine the role of TRAF6 in in-stent lesion formation after stent implantation in the rabbit carotid artery.
METHODS: Rabbit carotid arteries were injured with a 2F Fogarty catheter, and 28 days later, the same arteries were implanted with a 3-mm-diameter Palmaz-Schatz stent. A dominant negative (DN) form of TRAF6 (pME-FLAG-T6deltaRZ5) was then transferred using a plasmid-based electroporation method. Its effects were evaluated compared with the findings in arteries treated with control plasmid (pME-FLAG).
RESULTS: Immunostaining with anti-FLAG tag antibody showed that an expression plasmid vector containing the DN-TRAF6 sequence was successfully transferred to the arterial intima and media. Morphometric analyses revealed that the increase of intimal area in in-stent lesions was significantly inhibited by DN-TRAF6 14 days after stent implantation (DN-TRAF6 group, 3.01 +/- 0.25 x 10(5) microm2 vs control group, 4.25 +/- 0.23 x 10(5) microm2, P < .01), and the cell density was increased compared with that in the control group. In the DN-TRAF6 plasmid-treated vessels, cell replication was prevented in both the intima and media, and fewer leukocytes adhered to the luminal surface. Moreover, DN-TRAF6 suppressed macrophage infiltration, activation of proteases, and proteoglycan accumulation in the in-stent intima.
CONCLUSIONS: These findings suggest that TRAF6 plays an important role in cell replication, inflammatory cell infiltration, protease activity, and extracellular matrix accumulation that contributes to in-stent lesion development.
Takuya Miyahara; Hiroyuki Koyama; Tetsuro Miyata; Hiroshi Shigematsu; Jun-Ichiro Inoue; Tsuyoshi Takato; Hirokazu Nagawa
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of vascular surgery     Volume:  43     ISSN:  0741-5214     ISO Abbreviation:  J. Vasc. Surg.     Publication Date:  2006 Mar 
Date Detail:
Created Date:  2006-03-07     Completed Date:  2006-04-07     Revised Date:  2012-10-03    
Medline Journal Info:
Nlm Unique ID:  8407742     Medline TA:  J Vasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  592-600     Citation Subset:  IM    
Department of Vascular Regeneration, Graduate School of Medicine, The University of Tokyo, Hongo, Tokyo, Japan.
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MeSH Terms
Carotid Arteries / pathology*
Cell Count
Microscopy, Electron, Scanning
Microscopy, Electron, Transmission
Stents / adverse effects*
TNF Receptor-Associated Factor 6 / physiology*
Tunica Intima / pathology
Tunica Media / pathology
Reg. No./Substance:
0/TNF Receptor-Associated Factor 6

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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