Abstract:
:Neointima formation participates in the pathophysiology of atherosclerosis and restenosis. Proliferation and migration of vascular smooth muscle cells (VSMC) are initial responses to vascular injury. The aim of the present study was to assess the effect of gliotoxin, an inhibitor of nuclear factor (NF)-kappaB, on migration and proliferation of cultured rat VSMC and neointimal formation in injured rat vessels. In cultured VSMC, gliotoxin inhibited the nuclear translocation of the p65 subunit of NF-kappaB in response to inflammatory stimuli. In addition, gliotoxin inhibited VSMC migration and proliferation in response to platelet-derived growth factor-BB. This was associated with a rapid rearrangement of the F-actin and vimentin cytoskeleton. Furthermore, gliotoxin inhibited endothelial cell nuclear translocation of p65, cell surface expression of adhesion molecules such as VCAM-1, ICAM-1 and E-selectin, and monocytic cell adhesion to a cytokine-activated endothelial monolayer. In the rat carotid artery balloon catheter injury model, the systemic administration of gliotoxin for 10 days decreased neointimal hyperplasia and luminal stenosis by up to 90% and decreased the expression of proliferating cell nuclear antigen in the vessel wall by up to 70%, depending on the dose. These observations suggest that gliotoxin favorably regulates the response to vascular injury through actions on VSMC. However, further studies evaluating the therapeutic benefit of gliotoxin in restenosis after balloon angioplasty are required.
journal_name
J Vasc Resjournal_title
Journal of vascular researchauthors
Pozo M,Izquierdo MC,de Nicolás R,Egido J,Ortiz A,González-Cabrero Jdoi
10.1159/000176043subject
Has Abstractpub_date
2009-01-01 00:00:00pages
278-89issue
4eissn
1018-1172issn
1423-0135pii
000176043journal_volume
46pub_type
杂志文章abstract:BACKGROUND:Hypoxia results in pulmonary hypertension and vascular remodeling due to induction of pulmonary artery cell proliferation. Besides pulmonary artery smooth muscle cells, pulmonary artery endothelial cells (PAECs) are also involved in the development of pulmonary hypertension, but the effect of hypoxia on PAEC...
journal_title:Journal of vascular research
pub_type: 杂志文章
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journal_title:Journal of vascular research
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更新日期:2004-09-01 00:00:00
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pub_type: 杂志文章,随机对照试验
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pub_type: 杂志文章
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更新日期:2007-01-01 00:00:00
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pub_type: 杂志文章
doi:10.1159/000479873
更新日期:2017-01-01 00:00:00
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journal_title:Journal of vascular research
pub_type: 杂志文章
doi:10.1159/000159106
更新日期:1995-09-01 00:00:00
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journal_title:Journal of vascular research
pub_type: 杂志文章
doi:10.1159/000109818
更新日期:2008-01-01 00:00:00
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journal_title:Journal of vascular research
pub_type: 杂志文章
doi:10.1159/000158951
更新日期:1992-09-01 00:00:00
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journal_title:Journal of vascular research
pub_type: 杂志文章
doi:10.1159/000159008
更新日期:1993-09-01 00:00:00
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journal_title:Journal of vascular research
pub_type: 杂志文章
doi:10.1159/000090947
更新日期:2006-01-01 00:00:00
abstract::The D allele of the insertion (I)/deletion (D) polymorphism in the angiotensin-converting enzyme (ACE) gene and the C allele of the A1166-C polymorphism in the angiotensin II type 1 receptor (AGT1R) gene have been associated with altered vascular structure and with an increased risk of myocardial infarction. The aim o...
journal_title:Journal of vascular research
pub_type: 杂志文章
doi:10.1159/000025687
更新日期:1999-11-01 00:00:00
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journal_title:Journal of vascular research
pub_type: 杂志文章
doi:10.1159/000158994
更新日期:1993-07-01 00:00:00
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journal_title:Journal of vascular research
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更新日期:2014-01-01 00:00:00
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journal_title:Journal of vascular research
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journal_title:Journal of vascular research
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更新日期:1997-07-01 00:00:00
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更新日期:2007-01-01 00:00:00
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更新日期:1995-05-01 00:00:00
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journal_title:Journal of vascular research
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更新日期:1996-09-01 00:00:00
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journal_title:Journal of vascular research
pub_type: 杂志文章
doi:10.1159/000159222
更新日期:1997-05-01 00:00:00
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journal_title:Journal of vascular research
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更新日期:2008-01-01 00:00:00
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更新日期:2009-01-01 00:00:00