Document Detail


Heparanase regulates thrombosis in vascular injury and stent-induced flow disturbance.
MedLine Citation:
PMID:  22516446     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: The purpose of this study was to examine the role of heparanase in controlling thrombosis following vascular injury or endovascular stenting.
BACKGROUND: The use of endovascular stents are a common clinical intervention for the treatment of arteries occluded due to vascular disease. Both heparin and heparan sulfate are known to be potent inhibitors of thrombosis. Heparanase is the major enzyme that degrades heparan sulfate in mammalian cells. This study examined the role of heparanase in controlling thrombosis following vascular injury and stent-induced flow disturbance.
METHODS: This study used mice overexpressing human heparanase and examined the time to thrombosis using a laser-induced arterial thrombosis model in combination with vascular injury. An ex vivo system was used to examine the formation of thrombus to stent-induced flow disturbance.
RESULTS: In the absence of vascular injury, wild type and heparanase overexpressing (HPA Tg) mice had similar times to thrombosis in a laser-induced arterial thrombosis model. However, in the presence of vascular injury, the time to thrombosis was dramatically reduced in HPA Tg mice. An ex vivo system was used to flow blood from wild type and HPA Tg mice over stents and stented arterial segments from both animal types. These studies demonstrate markedly increased thromboses on stents with blood isolated from HPA Tg mice in comparison to blood from wild type animals. We found that blood from HPA Tg animals had markedly increased thrombosis when applied to stented arterial segments from either wild type or HPA Tg mice.
CONCLUSIONS: Taken together, this study's results indicate that heparanase is a powerful mediator of thrombosis in the context of vascular injury and stent-induced flow disturbance.
Authors:
Aaron B Baker; William J Gibson; Vijaya B Kolachalama; Mordechai Golomb; Laura Indolfi; Christopher Spruell; Eyal Zcharia; Israel Vlodavsky; Elazer R Edelman
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  59     ISSN:  1558-3597     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-04-20     Completed Date:  2012-06-14     Revised Date:  2014-10-16    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1551-60     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Angioplasty, Balloon / adverse effects*
Animals
Arterial Occlusive Diseases / enzymology,  etiology,  pathology
Biological Markers / analysis,  metabolism
Biopsy, Needle
Coronary Thrombosis / enzymology*,  etiology,  pathology
Disease Models, Animal
Endothelium, Vascular / injuries,  pathology
Glucuronidase / analysis,  metabolism*
Humans
Immunohistochemistry
Mice
Mice, Transgenic
Multivariate Analysis
Random Allocation
Risk Assessment
Sensitivity and Specificity
Stents / adverse effects*
Vascular System Injuries / enzymology*,  etiology,  pathology
Grant Support
ID/Acronym/Agency:
DP2 OD008716/OD/NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; EC 3.2.1.-/heparanase; EC 3.2.1.31/Glucuronidase
Comments/Corrections

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


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