Protein Kinase Cepsilon Expression in Platelets from Patients with Acute Myocardial Infarction
Academic Article
Publication Date:
2012
Short description:
Protein Kinase Cepsilon Expression in Platelets from Patients with Acute Myocardial Infarction / Carubbi, C., Mirandola, P., Mattioli, M., Galli, D., Marziliano, N., Merlini, P.A., Lina, D., Notarangelo, F., Cozzi, M.R., Gesi, M., Ardissino, D., DE MARCO, L., Vitale, M., Gobbi, G.. - In: PLOS ONE. - ISSN 1932-6203. - 7(10):(2012), p. e46409. [10.1371/journal.pone.0046409]
abstract:
Objective: 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.
(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.
Iris type:
1.1 Articolo in rivista
List of contributors:
Carubbi, Cecilia; Mirandola, Prisco; Mattioli, M.; Galli, Daniela; Marziliano, N.; Merlini, P. A.; Lina, D.; Notarangelo, F.; Cozzi, M. R.; Gesi, M.; Ardissino, D.; DE MARCO, L.; Vitale, Marco; Gobbi, Giuliana
Published in: