10.3389/fcvm.2020.00101.s003
Patricia B. Maguire
Patricia B.
Maguire
Martin E. Parsons
Martin E.
Parsons
Paulina B. Szklanna
Paulina B.
Szklanna
Monika Zdanyte
Monika
Zdanyte
Patrick Münzer
Patrick
Münzer
Madhumita Chatterjee
Madhumita
Chatterjee
Kieran Wynne
Kieran
Wynne
Dominik Rath
Dominik
Rath
Shane P. Comer
Shane P.
Comer
Melanie Hayden
Melanie
Hayden
Fionnuala Ní Áinle
Fionnuala Ní
Áinle
Meinrad Gawaz
Meinrad
Gawaz
Table_1_Comparative Platelet Releasate Proteomic Profiling of Acute Coronary Syndrome versus Stable Coronary Artery Disease.xlsx
Frontiers
2020
platelets
platelet releasate
proteomics
mass spectrometry
acute coronary syndrome
stable coronary artery disease
2020-06-24 12:59:23
Dataset
https://frontiersin.figshare.com/articles/dataset/Table_1_Comparative_Platelet_Releasate_Proteomic_Profiling_of_Acute_Coronary_Syndrome_versus_Stable_Coronary_Artery_Disease_xlsx/12555152
<p>Upon activation, platelets release a host of soluble and vesicular signals, collectively termed the “platelet releasate” (PR). The contents of this PR play a significant role in haemostasis, inflammation, and pathologic sequelae. Despite this, proteomic studies investigating the PR in coronary artery disease have not been performed. Here, we undertook a comparative label-free quantitative (LFQ) proteomic profiling of the 1 U/ml thrombin-induced PR from 13 acute coronary syndrome vs. 14 stable angina pectoris patients using a tandem mass spectrometry approach. Data are available via ProteomeXchange with identifier PXD009356. 318 PR proteins were identified across both cohorts with 9 proteins found to be differentially released, including tetranectin (CLEC3B), protein disulfide-isomerase-A3 (PDIA3), coagulation factor V (F5), and fibronectin (FN1). Strikingly, these 9 differential proteins were all associated with the gene ontology cellular component term “extracellular vesicle” and reduced levels of EVs were detected in the corresponding plasma of ST-segment elevation myocardial infarction (STEMI) patients. Network analysis revealed 3 proteins either reduced (F5; FN1) or absent (CLEC3B) in the PR of STEMI patients that are strongly connected to both the clotting cascade and major druggable targets on platelets. This moderated proteomic signature may prove useful for non-invasive risk assessment of the progression of coronary artery disease. These data further contribute to the growing evidence-base of using the platelet releasate as a predictor of pathological state and disease severity.</p>