scholarly journals IL-17A Facilitates Platelet Function through the ERK2 Signaling Pathway in Patients with Acute Coronary Syndrome

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e40641 ◽  
Author(s):  
Shuang Zhang ◽  
Jing Yuan ◽  
Miao Yu ◽  
Hong Fan ◽  
Zhang-Qiang Guo ◽  
...  
2019 ◽  
Vol 119 (10) ◽  
pp. 1563-1572 ◽  
Author(s):  
Stefan Stojkovic ◽  
Anne Yaël Nossent ◽  
Paul Haller ◽  
Bernhard Jäger ◽  
Kris G. Vargas ◽  
...  

AbstractMicroribonucleic acids (miRs) are small, noncoding ribonucleic acids (RNAs), which play an important role in the regulation of platelet function and activity. Several studies proposed a mechanistic role of platelet-related miRs in the pathophysiology of coronary artery disease (CAD) and atherothrombosis. Circulating, platelet-related miRs have been proposed as diagnostic, prognostic, as well as treatment response biomarkers in CAD and acute coronary syndrome (ACS). In this review, we summarize recent studies on the role of platelet-related miRs in the regulation of platelet function and activity. Furthermore, we review the studies investigating the role of platelet-related miRs as biomarkers in patients with CAD and ACS.


2016 ◽  
Vol 115 (02) ◽  
pp. 382-391 ◽  
Author(s):  
Jean-Philippe Collet ◽  
Mathieu Kerneis ◽  
Jean-Sebastien Hulot ◽  
Stephen A. O’Connor ◽  
Johanne Silvain ◽  
...  

SummaryOur aim was to demonstrate that the sequential use of the Verigene® rapid CYP2C19 test for genetic profiling and the VerifyNowTM bedside test for platelet function measurement in ACS patients may optimise P2Y12 inhibition. “Rapid” (CYP2C19*1/*1 or CYP2C19*17 carriers, n=211) and “slow” metabolisers (CYP2C19*2 carriers, n=58) were first put on clopidogrel and prasugrel for ≥ 2 weeks, respectively. Patients with low platelet reactivity (PRU< 30) on prasugrel or high platelet reactivity (> 208 PRU) on clopidogrel were then switched to clopidogrel and prasugrel, respectively. Our objectives were (i) to demonstrate that the proportion of “rapid” metabolisers on 75 mg of clopidogrel within 30–208 (PRU) of P2Y12 inhibition is non-inferior to “slow” metabolisers on prasugrel 10 mg and (ii) to evaluate the same end-point after switching drugs. The proportion of “rapid” and “slow” metabolisers within 30–208 PRU of P2Y12 inhibition was 71 % and 56.9 %, respectively, an absolute difference of +14.1 % (95 % CI, –0.05 % to 28.28 %) with a non-inferiority margin greater than the predefined margin of –10 %. Among patients out of target, all but one “slow” metabolisers displayed low-on prasugrel platelet reactivity while the majority of “rapid” metabolisers (68 %) displayed high-on clopidogrel platelet reactivity. After switching, the proportion of patients within 30–208 PRU of P2Y12 inhibition was 83.6 % and 79.3 % in “rapid” and “slow” metabolisers, respectively (+4.3 %, 95 % CI –7.3 % to 15.9 %). In conclusion, this study demonstrates a loose relationship between genotype and platelet function phenotype approaches but that they are complementary to select prasugrel or clopidogrel MD in stented ACS patients.


2006 ◽  
Vol 4 (12) ◽  
pp. 2547-2552 ◽  
Author(s):  
I. FUCHS ◽  
M. FROSSARD ◽  
A. SPIEL ◽  
E. RIEDMÜLLER ◽  
A. N. LAGGNER ◽  
...  

2019 ◽  
Vol 10 ◽  
Author(s):  
Xiaoye Li ◽  
Shuning Zhang ◽  
Zi Wang ◽  
Qiuyi Ji ◽  
Qibing Wang ◽  
...  

2014 ◽  
Vol 168 (5) ◽  
pp. 674-681.e1 ◽  
Author(s):  
Guillaume Cayla ◽  
Thomas Cuisset ◽  
Johanne Silvain ◽  
Patrick Henry ◽  
Florence Leclercq ◽  
...  

2012 ◽  
Vol 107 (06) ◽  
pp. 1122-1129 ◽  
Author(s):  
Mika Skeppholm ◽  
Fariborz Mobarrez ◽  
Karin Malmqvist ◽  
Håkan Wallén

SummaryAs microparticles are shedded upon platelet activation, and may be used to assess platelet function, we measured plasma concentrations of platelet-derived microparticles (PMPs) during and after an acute coronary syndrome (ACS). Fifty-one patients with ACS were investigated at admission, within 24 hours (before coronary angiography), and six months later. Sixty-one sex- and age-matched healthy controls were investigated once. PMPs were defined as particles <1.0 μm in size, negative to phalloidin (labels cell-fragments), and positive to CD61. Exposure of phosphatidylserine (PS+), CD62P and CD142 were also measured. Plasma concentrations of PS+PMPs exposing CD61, CD62P and CD142 were elevated 2.5, 6.0-, and 5.0-fold at admission (p<0.001 for all, compared to controls; aspirin only), decreased significantly 24 hours later following initiation of treatment with clopidogrel and subcutaneous anticoagulation (p<0.001 for all), and decreased even further six months later (p<0.01 for all). However, PS+PMPs exposing CD62P or CD142 were still between 1.2-and 2.3-fold higher than in controls (p<0.001 for both). The pattern for PS−PMPs during and after the ACS was very similar to that for PS+PMPs although the numbers were approximately 1/3 lower. In conclusion, PMP concentrations follow the pattern of platelet activation during and after an ACS. Decreased concentrations are observed after initiation of antithrombotic treatment, but PMP exposing CD62P or CD142 are still elevated after six months. Flow cytometric measurements of PMP in frozen-thawed samples enable studies of platelet function in larger clinical trials.


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