by Cecilia Carubbi, Prisco Mirandola, Maria Mattioli, Daniela Galli, Nicola Marziliano, Piera Angelica Merlini, Daniela Lina, Francesca Notarangelo, Maria Rita Cozzi, Marco Gesi, Diego Ardissino, Luigi De Marco, Marco Vitale, Giuliana Gobbi
Platelets play crucial roles in the pathophysiology of thrombosis and myocardial infarction. Protein kinase C e (PKCe) 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 PKCe in other species, we hypothesized that platelets from myocardial infarction patients might ectopically express PKCe with a pathophysiological role in the disease. Methods and Results
We therefore studied platelet PKCe 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 PKCe with a significant frequency as compared to both stable coronary artery disease and healthy subjects. PKCe returned negative during patient follow-up. The forced expression of PKCe in normal donor platelets significantly increased their response to adenosine diphosphate-induced activation and adhesion to subendothelial collagen. Conclusions
Our data suggest that platelet generations produced before the acute event retain PKCe-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.