Protein kinase C ε expression in platelets from patients with acute myocardial infarction.

<h4>Objective</h4>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 k...

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Autores principales:	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
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/8291358ed51c48708e8dd9477ad25d00
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spelling	oai:doaj.org-article:8291358ed51c48708e8dd9477ad25d002021-11-18T08:13:06ZProtein kinase C ε expression in platelets from patients with acute myocardial infarction.1932-620310.1371/journal.pone.0046409https://doaj.org/article/8291358ed51c48708e8dd9477ad25d002012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23071564/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Objective</h4>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.<h4>Methods and results</h4>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.<h4>Conclusions</h4>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.Cecilia CarubbiPrisco MirandolaMaria MattioliDaniela GalliNicola MarzilianoPiera Angelica MerliniDaniela LinaFrancesca NotarangeloMaria Rita CozziMarco GesiDiego ArdissinoLuigi De MarcoMarco VitaleGiuliana GobbiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 10, p e46409 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q 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 Protein kinase C ε expression in platelets from patients with acute myocardial infarction.
description	<h4>Objective</h4>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.<h4>Methods and results</h4>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.<h4>Conclusions</h4>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.
format	article
author	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
author_facet	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
author_sort	Cecilia Carubbi
title	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_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_sort	protein kinase c ε expression in platelets from patients with acute myocardial infarction.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/8291358ed51c48708e8dd9477ad25d00
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Protein kinase C ε expression in platelets from patients with acute myocardial infarction.

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