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

OBJECTIVE: 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...

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Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3465320/
https://www.ncbi.nlm.nih.gov/pubmed/23071564
http://dx.doi.org/10.1371/journal.pone.0046409
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author 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
author_facet 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
author_sort Carubbi, Cecilia
collection PubMed
description OBJECTIVE: 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. METHODS AND RESULTS: 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. CONCLUSIONS: 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.
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spelling pubmed-34653202012-10-15 Protein Kinase C ε Expression in Platelets from Patients with Acute Myocardial Infarction 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 PLoS One Research Article OBJECTIVE: 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. METHODS AND RESULTS: 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. CONCLUSIONS: 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. Public Library of Science 2012-10-05 /pmc/articles/PMC3465320/ /pubmed/23071564 http://dx.doi.org/10.1371/journal.pone.0046409 Text en © 2012 Carubbi et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
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
Protein Kinase C ε Expression in Platelets from Patients with Acute Myocardial Infarction
title Protein Kinase C ε Expression in Platelets from Patients with Acute Myocardial Infarction
title_full Protein Kinase C ε Expression in Platelets from Patients with Acute Myocardial Infarction
title_fullStr Protein Kinase C ε Expression in Platelets from Patients with Acute Myocardial Infarction
title_full_unstemmed Protein Kinase C ε Expression in Platelets from Patients with Acute Myocardial Infarction
title_short Protein Kinase C ε Expression in Platelets from Patients with Acute Myocardial Infarction
title_sort protein kinase c ε expression in platelets from patients with acute myocardial infarction
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3465320/
https://www.ncbi.nlm.nih.gov/pubmed/23071564
http://dx.doi.org/10.1371/journal.pone.0046409
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