ArticlePloS one2012
Protein kinase C ε expression in platelets from patients with acute myocardial infarction.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- State-Dependent DNA Methylation Signatures Distinguish Acute from Stable Coronary Syndromes.International journal of molecular sciences · 2026Article
- How Protein Depletion Balances Thrombosis and Bleeding Risk in the Context of Platelet's Activatory and Negative Signaling.International journal of molecular sciences · 2024Review
- Sodium-glucose cotransporter 2 inhibitors antagonize lipotoxicity in human myeloid angiogenic cells and ADP-dependent activation in human platelets: potential relevance to prevention of cardiovascular events.Cardiovascular diabetology · 2020Article
- Sighting acute myocardial infarction through platelet gene expression.Scientific reports · 2019Article
- Combination of Platelet expression of PKCepsilon and cardiac troponin-I for early diagnosis of chest pain patients in the emergency department.Scientific reports · 2019Article
- Platelet expression of PKCepsilon oncoprotein in myelofibrosis is associated with disease severity and thrombotic risk.Annals of translational medicine · 2017Article
- Human thrombopoiesis depends on Protein kinase Cδ/protein kinase Cε functional couple.Haematologica · 2016Article
- Article
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Authors and funding
14 authors.
Funding
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Abstract
objectivePlatelets play crucial roles in the pathophysiology of thrombosis and myocardial infarction. Protein kinase C ε (PKCε) is virtually absent in human platelets and its expression is precisely regulated during human megakaryocytic differentiation. On the basis of what is known on the role of platelet PKCε in other species, we hypothesized that platelets from myocardial infarction patients might ectopically express PKCε with a pathophysiological role in the disease. METHODS AND
resultsWe therefore studied platelet PKCε expression from 24 patients with myocardial infarction, 24 patients with stable coronary artery disease and 24 healthy subjects. Indeed, platelets from myocardial infarction patients expressed PKCε with a significant frequency as compared to both stable coronary artery disease and healthy subjects. PKCε returned negative during patient follow-up. The forced expression of PKCε in normal donor platelets significantly increased their response to adenosine diphosphate-induced activation and adhesion to subendothelial collagen.
conclusionsOur data suggest that platelet generations produced before the acute event retain PKCε-mRNA that is not down-regulated during terminal megakaryocyte differentiation. Results are discussed in the perspective of peri-infarctual megakaryocytopoiesis as a critical component of myocardial infarction pathophysiology.
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