Document Detail

Carbon monoxide-induced early thrombolysis contributes to heme oxygenase-1-mediated inhibition of neointimal growth after vascular injury in hypercholesterolemic mice.
MedLine Citation:
PMID:  16783602     Owner:  NLM     Status:  MEDLINE    
Arterial thrombosis is a critical event in the pathogenesis of lesion development. In this study, we evaluated the effect of heme oxygenase-1 (HO-1), a stress-inducible enzyme with vasoprotective functions, on arterial thrombosis following vascular mechanical injury. The carotid arteries of apoE-deficient mice were subjected to angioplasty with a modified beaded-needle. Arterial thrombosis occurred at 12 h after injury. Treatment of the injured vessels with an adenovirus bearing HO-1 gene (Adv-HO-1) (1 x 10(8) pfu), but not saline or empty adenovirus (Adv), immediately after angioplasty resulted in earlier thrombolysis and restoration of blood flow detected at 24 h. Immunohistochemistry revealed that the arterial plasminogen activator inhibitor-1 (PAI-1) expression was markedly reduced in Adv-HO-1-treated injured arteries as compared to control counterparts. The thrombolytic effect was also observed by exposing animals with existing arterial thrombosis to carbon monoxide (CO) (250 ppm, 2 h), a byproduct derived from heme degradation by HO-1. In parallel with less fibrin(ogen) deposition, the macrophage infiltration, monocyte chemoattractant protein-1 expression and neointimal formation assessed at 2 weeks after angioplasty were substantially reduced in injured arteries treated with Adv-HO-1. These results support a role of early thrombolysis induced by CO in HO-1-mediated protection against intimal hyperplasia after vascular injury.
Yen-Hui Chen; Hui-Ling Tsai; Ming-Tsai Chiang; Lee-Young Chau
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-06-17
Journal Detail:
Title:  Journal of biomedical science     Volume:  13     ISSN:  1021-7770     ISO Abbreviation:  J. Biomed. Sci.     Publication Date:  2006 Sep 
Date Detail:
Created Date:  2006-09-29     Completed Date:  2007-01-24     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9421567     Medline TA:  J Biomed Sci     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  721-30     Citation Subset:  IM    
Institute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan, Republic of China.
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MeSH Terms
Apolipoproteins E / deficiency
Carbon Monoxide / physiology*
Carotid Artery, Common / physiopathology*
Fibrin / metabolism
Fibrinogen / metabolism
Heme Oxygenase-1 / genetics,  physiology*
Hypercholesterolemia / physiopathology*
Inflammation / metabolism,  physiopathology
Muscle Development
Muscle, Smooth, Vascular / growth & development
Plasminogen Activator Inhibitor 1 / metabolism
Thrombosis / physiopathology*
Transduction, Genetic
Reg. No./Substance:
0/Apolipoproteins E; 0/Plasminogen Activator Inhibitor 1; 630-08-0/Carbon Monoxide; 9001-31-4/Fibrin; 9001-32-5/Fibrinogen; EC Oxygenase-1

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

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