TY - JOUR
T1 - Sighting acute myocardial infarction through platelet gene expression
AU - Gobbi, Giuliana
AU - Carubbi, Cecilia
AU - Tagliazucchi, Guidantonio Malagoli
AU - Masselli, Elena
AU - Mirandola, Prisco
AU - Pigazzani, Filippo
AU - Crocamo, Antonio
AU - Notarangelo, Maria Francesca
AU - Suma, Sergio
AU - Paraboschi, Elvezia
AU - Maglietta, Giuseppe
AU - Nagalla, Srikanth
AU - Pozzi, Giulia
AU - Galli, Daniela
AU - Vaccarezza, Mauro
AU - Fortina, Paolo
AU - Addya, Sankar
AU - Ertel, Adam
AU - Bray, Paul
AU - Duga, Stefano
AU - Berzuini, Carlo
AU - Vitale, Marco
AU - Ardissino, Diego
N1 - Funding Information:
This work was supported by Programma di ricerca Regione-Università, Regione Emilia-Romagna, bando Ricerca Innovativa 2010–2012 “Cardiovascular genetics: from bench to bedside - Genomics & transcriptomics of ischemic heart disease” - CUP E35E09000880002.
Publisher Copyright:
© 2019, The Author(s).
PY - 2019/12/1
Y1 - 2019/12/1
N2 - Acute myocardial infarction is primarily due to coronary atherosclerotic plaque rupture and subsequent thrombus formation. Platelets play a key role in the genesis and progression of both atherosclerosis and thrombosis. Since platelets are anuclear cells that inherit their mRNA from megakaryocyte precursors and maintain it unchanged during their life span, gene expression profiling at the time of an acute myocardial infarction provides information concerning the platelet gene expression preceding the coronary event. In ST-segment elevation myocardial infarction (STEMI), a gene-by-gene analysis of the platelet gene expression identified five differentially expressed genes: FKBP5, S100P, SAMSN1, CLEC4E and S100A12. The logistic regression model used to combine the gene expression in a STEMI vs healthy donors score showed an AUC of 0.95. The same five differentially expressed genes were externally validated using platelet gene expression data from patients with coronary atherosclerosis but without thrombosis. Platelet gene expression profile highlights five genes able to identify STEMI patients and to discriminate them in the background of atherosclerosis. Consequently, early signals of an imminent acute myocardial infarction are likely to be found by platelet gene expression profiling before the infarction occurs.
AB - Acute myocardial infarction is primarily due to coronary atherosclerotic plaque rupture and subsequent thrombus formation. Platelets play a key role in the genesis and progression of both atherosclerosis and thrombosis. Since platelets are anuclear cells that inherit their mRNA from megakaryocyte precursors and maintain it unchanged during their life span, gene expression profiling at the time of an acute myocardial infarction provides information concerning the platelet gene expression preceding the coronary event. In ST-segment elevation myocardial infarction (STEMI), a gene-by-gene analysis of the platelet gene expression identified five differentially expressed genes: FKBP5, S100P, SAMSN1, CLEC4E and S100A12. The logistic regression model used to combine the gene expression in a STEMI vs healthy donors score showed an AUC of 0.95. The same five differentially expressed genes were externally validated using platelet gene expression data from patients with coronary atherosclerosis but without thrombosis. Platelet gene expression profile highlights five genes able to identify STEMI patients and to discriminate them in the background of atherosclerosis. Consequently, early signals of an imminent acute myocardial infarction are likely to be found by platelet gene expression profiling before the infarction occurs.
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U2 - 10.1038/s41598-019-56047-0
DO - 10.1038/s41598-019-56047-0
M3 - Article
C2 - 31863085
AN - SCOPUS:85076919837
SN - 2045-2322
VL - 9
JO - Scientific Reports
JF - Scientific Reports
IS - 1
M1 - 19574
ER -