Protein Kinase C ε Expression in Platelets from Patients with Acute Myocardial Infarction

• Published in: PloS one Vol. 7; no. 10; p. e46409
• Main Authors: Carubbi, Cecilia, Mirandola, Prisco, Mattioli, Maria, Galli, Daniela, Marziliano, Nicola, Merlini, Piera Angelica, Lina, Daniela, Notarangelo, Francesca, Cozzi, Maria Rita, Gesi, Marco, Ardissino, Diego, De Marco, Luigi, Vitale, Marco, Gobbi, Giuliana
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 05.10.2012; Public Library of Science (PLoS)
• Subjects: Acute coronary syndromes; Adenosine; Adenosine diphosphate; Aged; Angina pectoris; Angioplasty; Base Sequence; Biology; Blood clots; Blood platelets; Blood Platelets - enzymology; Cardiology; Case-Control Studies; Collagen; Coronary artery; Coronary artery disease; Differentiation; DNA Primers; DNA, Complementary; Female; Flow Cytometry; Gene expression; Heart attacks; Heart diseases; Humans; Kinases; Laboratories; Male; Medicine; mRNA; Myocardial infarction; Myocardial Infarction - blood; Myocardial Infarction - enzymology; Patients; Phosphorylation; Platelet Activation; Platelets; Protein kinase C; Protein Kinase C-epsilon - blood; Protein Kinase C-epsilon - genetics; Protein synthesis; Proteins; Real-Time Polymerase Chain Reaction; Thromboembolism; Thrombosis; Italy
• DOI: 10.1371/journal.pone.0046409
• ISSN: 1932-6203

Platelets 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. We 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. Our 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.