Document Detail


Induction of platelet aggregation after a direct physical interaction with diesel exhaust particles.
MedLine Citation:
PMID:  23206187     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: There is a proven link between exposure to traffic-derived particulate air pollution and the incidence of platelet-driven cardiovascular diseases. It is suggested that inhalation of small, nanosized particles increases cardiovascular risk via toxicological and inflammatory processes and translocation of nanoparticles into the bloodstream has been shown in experimental models. We therefore investigated the ability of diesel exhaust particles (DEP) to interact physically and functionally with platelets.
METHODS: The interaction of DEP and carbon black (CB) with platelets was examined by transmission electron microscopy (TEM), whereas the functional consequences of exposure were assessed by measuring in vitro and in vivo platelet aggregation via established methods.
RESULTS: Both DEP and CB were internalized and seen in proximity with the open canalicular system in platelets. DEP induced platelet aggregation in vitro whereas CB had no effect. DEP induced Ca(2+) release, dense granule secretion and surface P-selectin expression, but not toxicologic membrane disruption. Low concentrations of DEP potentiated agonist-induced platelet aggregation in vitro and in vivo.
CONCLUSIONS: DEP associate physically with platelets in parallel with a Ca(2+) -mediated aggregation response displaying the conventional features of agonist-induced aggregation. The ability of DEP to enhance the aggregation response to platelet stimuli would be expected to increase the incidence of platelet-driven cardiovascular events should they be inhaled and translocate into the blood. This study provides a potential mechanism for the increased thrombotic risk associated with exposure to ambient particulate air pollution.
Authors:
A Solomon; E Smyth; N Mitha; S Pitchford; A Vydyanath; P K Luther; A J Thorley; T D Tetley; M Emerson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of thrombosis and haemostasis : JTH     Volume:  11     ISSN:  1538-7836     ISO Abbreviation:  J. Thromb. Haemost.     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-02-12     Completed Date:  2013-08-22     Revised Date:  2014-02-20    
Medline Journal Info:
Nlm Unique ID:  101170508     Medline TA:  J Thromb Haemost     Country:  England    
Other Details:
Languages:  eng     Pagination:  325-34     Citation Subset:  IM    
Copyright Information:
© 2012 International Society on Thrombosis and Haemostasis.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Platelets / drug effects*,  metabolism,  ultrastructure
Calcium / metabolism
Dose-Response Relationship, Drug
Humans
Male
Mice
Mice, Inbred BALB C
Microscopy, Electron, Transmission
Nanoparticles*
P-Selectin / metabolism
Platelet Aggregation / drug effects*
Platelet Function Tests
Soot / metabolism,  toxicity*
Time Factors
Vehicle Emissions / toxicity*
Grant Support
ID/Acronym/Agency:
G0700926//Medical Research Council; PG/10/80/28605//British Heart Foundation; RG/11/21/29335//British Heart Foundation
Chemical
Reg. No./Substance:
0/P-Selectin; 0/SELP protein, human; 0/Soot; 0/Vehicle Emissions; SY7Q814VUP/Calcium

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


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