Front cover: 2D-DIGE-based proteomic analysis of intracoronary versus peripheral arterial blood platelets from acute myocardial infarction patients: Upregulation of platelet activation biomarkers at the culprit site

2016 ◽  
Vol 10 (8) ◽  
pp. NA-NA
Author(s):  
Paula Vélez ◽  
Raymundo Ocaranza-Sánchez ◽  
Diego López-Otero ◽  
Lilian Grigorian-Shamagian ◽  
Isaac Rosa ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Activation ◽  
Proteomic Analysis ◽  
Blood Platelets ◽  
Front Cover ◽  
2D Dige ◽  
Arterial Blood ◽  
Peripheral Arterial

Abstract 803: Diesel Exhaust Inhalation Enhances Thrombus Formation In Man

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Andrew J Lucking ◽  
Magnus Lundback ◽  
Nicholas L Mills ◽  
Dana Faratian ◽  
Fleming Cassee ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Air Pollution ◽  
Platelet Activation ◽  
Diesel Exhaust ◽  
Intermittent Exercise ◽  
Ex Vivo ◽  
Thrombus Formation ◽  
Ex Vivo Model ◽  
Double Blind

Background: Transient exposure to traffic-derived air pollution may be a trigger for acute myocardial infarction although the mechanism is unclear. The aim of this study was to investigate the effect of diesel exhaust inhalation on thrombus formation in man using an ex vivo model of thrombosis. Methods and Results: In a double-blind randomized cross-over study, 20 healthy volunteers were exposed to diluted diesel exhaust (300 μg/m3) or filtered air during intermittent exercise for 1 or 2 hours. Thrombus formation, coagulation, platelet activation and inflammatory markers were measured at 2 and 6 hours after exposure. Thrombus formation was measured using the Badimon ex vivo perfusion chamber at low (212 /s) and high (1,690 /s) shear rates with porcine aortic tunica media as the thrombogenic substrate. Specimens were fixed, stained and thrombus area measured using computerized planimetry. Compared to filtered air, diesel exhaust increased thrombus formation in the low and high shear chambers by 24.2% (p<0.001) and 19.1% (p<0.001) respectively. This increased thrombogenicity was seen at two and six hours, and using two different types of diesel exposure. Although there were no effects on coagulation variables, diesel exhaust inhalation increased platelet-neutrophil (6.5% to 9.2%; P<0.05) and platelet-monocyte (21.0% to 25.0%; P<0.05) aggregates 2 hours following exposure. Conclusions: Inhalation of diesel exhaust increases ex vivo thrombus formation and causes platelet activation in man. These findings provide a potential mechanism that links exposure to traffic-derived air pollution with acute atherothrombotic events including acute myocardial infarction.

Abstract 53: Ablation of Thrombin Signaling in Platelets but Not in Endothelial Cells Impairs Hemostasis in a Mouse Model of Spontaneous Gastrointestinal Bleeding

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Stephen J Wilson ◽  
Maria M Stevens ◽  
Shaun R Coughlin
Keyword(s):  
Myocardial Infarction ◽  
Endothelial Cells ◽  
Platelet Activation ◽  
Bleeding Risk ◽  
Arterial Disease ◽  
Gi Bleeding ◽  
Intestinal Polyposis ◽  
Wild Type ◽  
Spontaneous Bleeding ◽  
Peripheral Arterial

Human PAR1 is expressed in endothelial cells as well as in platelets where it facilitates the response to thrombin and platelet activation. Vorapaxar, a PAR1 antagonist, prevents myocardial infarction and stroke in patients with prior MI or peripheral arterial disease at a cost of increased bleeding risk. Par1 is also highly expressed in endothelial cells in mice, and Par1-deficiency is associated with bleeding in the mouse embryo at midgestation. Additionally, known actions of endothelial PAR1 activation suggest pro-hemostatic functions. This raises the question of whether inhibition of PAR1 function in endothelial cells (in addition to PAR1 inhibition in platelets) contributes to the bleeding risk associated with Vorapaxar treatment. Our previous work demonstrated that Par1 deficiency results in loss of thrombin signaling in mouse endothelial cells but not mouse platelets, while Par4 deficiency ablated thrombin-induced platelet activation in mice. Thus, mice allow us to separate loss of thrombin signaling in platelets from loss of thrombin signaling in endothelial cells. Accordingly, we used Apc min/+ mice, which develop intestinal polyposis and spontaneous GI bleeding, as a model to determine whether loss of thrombin signaling in platelets (Par4 KO) or endothelial and other cells (Par1 KO) exacerbates spontaneous bleeding. Hematocrit and other hematologic parameters were measured biweekly from 7 weeks through 15 weeks of age. Hematocrits in mice wild-type for Apc were stable over this period (41.48 ± 0.48 at 7 weeks; 40.48 ± 0.37 at 15 weeks, n=15). Hematocrits in Apc min/+ mice fell approximately linearly from 37.06 ± 0.82 at 7 weeks to 14.39 ± 1.12 at 15 weeks (n=15). Hematocrits in Par1-deficient Apc min/+ mice were indistinguishable from those in Apc min/+ without Par deficiency (14.39 ± 1.12 vs 14.47 ± 1.66 at 15 weeks; n=6-15). By contrast, Par4-deficient Apc min/+ mice were already severely anemic at 7 weeks compared to Apc min/+ mice (19 ± 2.0 vs 39 ± 3.6; p<0.01, n=4). Par-dependent differences in polyp count and size were not detected. Taken together, our results suggest that loss of thrombin signaling in platelets promotes spontaneous GI bleeding in the Apc min model while loss of thrombin signaling in endothelial cells is without effect in this system.

Combined Thrombolysis with Abciximab Favourably Influences Platelet-Leukocyte Interactions and Platelet Activation in Acute Myocardial Infarction

2005 ◽  
Vol 20 (3) ◽  
pp. 155-161 ◽  
Author(s):  
Sebastian Szabo ◽  
Diana Etzel ◽  
Raila Ehlers ◽  
Thomas Walter ◽  
Silke Kazmaier ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Activation

Proteomic analysis of plasma samples from patients with acute myocardial infarction identifies haptoglobin as a potential prognostic biomarker

2011 ◽  
Vol 75 (1) ◽  
pp. 229-236 ◽  
Author(s):  
Benjamin Haas ◽  
Tommaso Serchi ◽  
Daniel R. Wagner ◽  
Georges Gilson ◽  
Sebastien Planchon ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Proteomic Analysis ◽  
Prognostic Biomarker ◽  
Plasma Samples
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