scholarly journals The colonic metabolites dihydrocaffeic acid and dihydroferulic acid are more effective inhibitors of in vitro platelet activation than their phenolic precursors

2017 ◽  
Vol 8 (3) ◽  
pp. 1333-1342 ◽  
Author(s):  
Gema Baeza ◽  
Eva-Maria Bachmair ◽  
Sharon Wood ◽  
Raquel Mateos ◽  
Laura Bravo ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Platelet Activation ◽  
Morbidity And Mortality ◽  
In Vitro Platelet Activation

Cardiovascular disease (CVD) is the major cause of morbidity and mortality worldwide.

Methicillin-Resistant Staphylococcus aureus Induces In Vitro Platelet Activation and a Procoagulant Respons

CHEST Journal ◽  
2011 ◽  
Vol 140 (4) ◽  
pp. 991A
Author(s):  
Zechariah Franks ◽  
Robert Campbell ◽  
Andy Weyrich ◽  
Guy Zimmerman ◽  
Matthew Rondina
Keyword(s):  
Staphylococcus Aureus ◽  
Platelet Activation ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
Methicillin Resistant ◽  
In Vitro Platelet Activation

Inhibitory effects of lycopene on in vitro platelet activation and in vivo prevention of thrombus formation

2005 ◽  
Vol 146 (4) ◽  
pp. 216-226 ◽  
Author(s):  
George Hsiao ◽  
Ying Wang ◽  
Nien-Hsuan Tzu ◽  
Tsorng-Hang Fong ◽  
Ming-Yi Shen ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Thrombus Formation ◽  
Inhibitory Effects ◽  
In Vitro Platelet Activation

Lack of effect of isradipine on in vitro platelet activation

1993 ◽  
Vol 72 (4) ◽  
pp. 373-375
Author(s):  
Julio B Fernandes ◽  
Ulhas P Naik ◽  
Mariana S Markell ◽  
Elizabeth Kornecki
Keyword(s):  
Platelet Activation ◽  
In Vitro Platelet Activation

scholarly journals Epigenetic regulation of PAR4-related platelet activation: mechanistic links between environmental exposure and cardiovascular disease

2018 ◽  
Author(s):  
Laura J. Corbin ◽  
Amy E. Taylor ◽  
Stephen J. White ◽  
Christopher M. Williams ◽  
Kurt Taylor ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Dna Methylation ◽  
Platelet Activation ◽  
Cardiovascular Health ◽  
Platelet Reactivity ◽  
Dna Hypomethylation ◽  
Enhancer Activity ◽  
Exon 2 ◽  
Short Term Exposure

AbstractProtease-activated receptor 4 (PAR4) is a potent thrombin receptor. Epigenetic control of theF2RL3locus (which encodes for PAR4) via DNA methylation is associated with both smoking and cardiovascular disease. We examined the association between DNA hypomethylation atF2RL3and risk of cardiovascular disease, focusing on acute myocardial infarction (AMI) (n=853 cases / 2,352 controls). We usedin vitrocell models to dissect the role of DNA methylation in regulating expression ofF2RL3.We investigated the interplay betweenF2RL3DNA methylation and platelet function in human (n=41). Lastly, we used Mendelian randomization to unify observational and functional work by assessing evidence for causal relationships using data from UK Biobank (n=407,141) and CARDIoGRAMplusC4D (n=184,305). Observationally, one standard deviation (SD) decrease in DNA methylation atF2RL3was associated with a 25% increase in the odds of AMI.In vitro, short-term exposure of cells to cigarette smoke reducedF2RL3DNA methylation and increased gene expression. Transcriptional assays flagged a role for a CEBP recognition sequence in modulating the enhancer activity ofF2RL3exon 2. Lower DNA methylation atF2RL3was associated with increased platelet reactivity in human. The estimated casual odds ratio of ischaemic heart disease was 1.03 (95% CI: 1.00, 1.07) per 1 SD decrease inF2RL3DNA. In conclusion, we show that DNA methylation-dependent platelet activation is part of a complex system of features contributing to cardiovascular health. Tailoring therapeutic intervention to new knowledge ofF2RL3/PAR4 function should be explored to ameliorate the detrimental effects of this risk factor on cardiovascular health.One sentence summaryDNA methylation-dependent platelet activation is a likely causal contributor to cardiovascular health.

scholarly journals Signaling through FcγRIIA and the C5a-C5aR pathway mediates platelet hyperactivation in COVID-19

2021 ◽  
Author(s):  
Sokratis A. Apostolidis ◽  
Amrita Sarkar ◽  
Heather M. Giannini ◽  
Rishi R. Goel ◽  
Divij Mathew ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Platelet Activation ◽  
Clinical Manifestations ◽  
Vascular Complications ◽  
Surface Expression ◽  
Microfluidic Chamber ◽  
Mediators Of Inflammation ◽  
Syk Inhibitor

Patients with COVID-19 present with a wide variety of clinical manifestations. Thromboembolic events constitute a significant cause of morbidity and mortality in patients infected with SARS-CoV-2. Severe COVID-19 has been associated with hyperinflammation and pre-existing cardiovascular disease. Platelets are important mediators and sensors of inflammation and are directly affected by cardiovascular stressors. In this report, we found that platelets from severely ill, hospitalized COVID-19 patients exhibit higher basal levels of activation measured by P-selectin surface expression, and have a poor functional reserve upon in vitro stimulation. Correlating clinical features to the ability of plasma from COVID-19 patients to stimulate control platelets identified ferritin as a pivotal clinical marker associated with platelet hyperactivation. The COVID-19 plasma-mediated effect on control platelets was highest for patients that subsequently developed inpatient thrombotic events. Proteomic analysis of plasma from COVID-19 patients identified key mediators of inflammation and cardiovascular disease that positively correlated with in vitro platelet activation. Mechanistically, blocking the signaling of the FcγRIIa-Syk and C5a-C5aR pathways on platelets, using antibody-mediated neutralization, IgG depletion or the Syk inhibitor fostamatinib, reversed this hyperactivity driven by COVID-19 plasma and prevented platelet aggregation in endothelial microfluidic chamber conditions, thus identifying these potentially actionable pathways as central for platelet activation and/or vascular complications in COVID-19 patients. In conclusion, we reveal a key role of platelet-mediated immunothrombosis in COVID-19 and identify distinct, clinically relevant, targetable signaling pathways that mediate this effect. These studies have implications for the role of platelet hyperactivation in complications associated with SARS-CoV-2 infection.

Iohexol, platelet activation and thrombosis

1998 ◽  
Vol 39 (4) ◽  
pp. 349-354 ◽  
Author(s):  
K. S. Sakariassen ◽  
R. M. Barstad ◽  
M. J. A. G. Hamers ◽  
H. Stormorken
Keyword(s):  
Platelet Activation ◽  
Arterial Wall ◽  
Ex Vivo ◽  
Thrombus Formation ◽  
Human Model ◽  
Intravascular Thrombosis ◽  
Platelet Thrombus ◽  
In Vitro Platelet Activation ◽  
Platelet Secretion

Background: The nonionic monomer iohexol triggers in vitro platelet secretion of β-thromboglobulin (β-TG). This iohexol platelet activation may promote intravascular thrombosis. We studied this relationship by employing a human model of collagen-induced platelet thrombus formation at arterial flow. The ionic dimer ioxaglate, the nonionic dimer iodixanol, and glucose were included. Methods and Results: In vitro platelet activation as measured by β-TG secretion following a 1-min incubation of native blood with 50 vol% of iohexol was significant. Glucose solutions of 300, 580 and 825 mosmol, corresponding to the osmolalities of respectively iodixanol, ioxaglate and iohexol, increased the β-TG secretion in parallel with the osmolalities. Ioxaglate and iodixanol were virtually inert. Continuous infusion of iohexol or 580 or 825 mosmol glucose (40 vol%) into flowing native blood at an arterial wall shear rate of 2600 s−1 in an ex vivo collagen-induced platelet thrombus formation device triggered pronounced secretion of β-TG. However, the platelet thrombus formation in blood mixed with iohexol was within the same range as that observed with ioxaglate or iodixanol. Increasing glucose osmolality induced increasing β-TG secretion, which paralleled gradually decreasing platelet thrombus formation. Conclusion: Iohexol and 580 or 825 mosmol glucose trigger platelet secretion of β-TG. This secretion is not associated with enhanced collagen-induced platelet thrombus formation at high arterial shear.

Microparticle generation during in vitro platelet activation by anti-CD9 murine monoclonal antibodies

1991 ◽  
Vol 62 (5) ◽  
pp. 429-439 ◽  
Author(s):  
Shosaku Nomura ◽  
Hirokazu Nagata ◽  
Masahiko Suzuki ◽  
Koji Kondo ◽  
Shigetoshi Ohga ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Platelet Activation ◽  
Murine Monoclonal Antibodies ◽  
In Vitro Platelet Activation

Inhibitory effects of hydrogen on in vitro platelet activation and in vivo prevention of thrombosis formation

Life Sciences ◽  
2019 ◽  
Vol 233 ◽  
pp. 116700 ◽  
Author(s):  
Yun Wang ◽  
Ya-ping Wu ◽  
Ji-ju Han ◽  
Mao-qing Zhang ◽  
Chen-xi Yang ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Inhibitory Effects ◽  
Prevention Of Thrombosis ◽  
In Vitro Platelet Activation

Thrombospondin-1: a unique marker to identify in vitro platelet activation when monitoring in vivo processes

2010 ◽  
Vol 8 (8) ◽  
pp. 1809-1819 ◽  
Author(s):  
P. STARLINGER ◽  
H. P. MOLL ◽  
A. ASSINGER ◽  
C. NEMETH ◽  
K. HOETZENECKER ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Thrombospondin 1 ◽  
In Vitro Platelet Activation
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