Transcriptional fingerprint of human whole blood at the site of coronary occlusion in acute myocardial infarction

Olivier Muller, Leen Delrue, Michalis Hamilos, Steven Vercauteren, Argyrios Ntalianis, Catalina Trana, Fabio Mangiacapra, Karen Dierickx, Bernard De Bruyne, William Wijns, Atta Behfar, Emanuele Barbato, Andre Terzic, Marc Vanderheyden, Jozef Bartunek

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Aims: Transcriptome patterns associated with acute myocardial infarction at the site of coronary occlusion are largely unknown. The aim of this study was to decipher the angiogenic, atherosclerotic, and inflammatory mRNA profiles in whole blood samples collected at the site of coronary occlusion in patients with ST-elevation myocardial infarction (STEMI). Methods and results: In five consecutive patients with STEMI, blood was sampled at the site of occlusion (local) and in the systemic circulation (peripheral) during primary percutaneous coronary intervention. RNA was extracted from whole blood samples. Among 221 genes involved in angiogenesis, inflammation and atherosclerosis, 24 were shown to be differentially modulated locally, by analysis with custom-designed DNA array technology. Validation in 28 distinct STEMI patients using real-time quantitative PCR identified seven out of these 24 genes to be consistently and significantly upregulated in local versus peripheral blood (p<0.05). Three genes were chemokine family members (CCL2, CCL18 and CXCL12), three genes belonged to the cell-cell and cell-extracellular matrix family (FN1, CDH5 and SPP1), and one gene was representative of the lipoprotein family (APOE). Conclusions: We identified a set of whole blood transcripts induced at the site of coronary occlusion in the acute phase of myocardial infarction. Resolved genes indicate a predominant role for chemokines, cell-extracellular matrix, and lipoprotein alterations in the pathophysiology of acute myocardial infarction and the initial response to myocardial injury.

Original languageEnglish (US)
Pages (from-to)458-466
Number of pages9
JournalEuroIntervention
Volume7
Issue number4
DOIs
StatePublished - Aug 2011

Fingerprint

Coronary Occlusion
Dermatoglyphics
Myocardial Infarction
Genes
Chemokines
Lipoproteins
Extracellular Matrix
Percutaneous Coronary Intervention
Oligonucleotide Array Sequence Analysis
Transcriptome
Real-Time Polymerase Chain Reaction
Atherosclerosis
RNA
Inflammation
Technology
Messenger RNA
Wounds and Injuries
ST Elevation Myocardial Infarction

Keywords

  • Cytokines
  • Gene expression
  • Myocardial infarction
  • STEMI

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Muller, O., Delrue, L., Hamilos, M., Vercauteren, S., Ntalianis, A., Trana, C., ... Bartunek, J. (2011). Transcriptional fingerprint of human whole blood at the site of coronary occlusion in acute myocardial infarction. EuroIntervention, 7(4), 458-466. https://doi.org/10.4244/EIJV7I4A75

Transcriptional fingerprint of human whole blood at the site of coronary occlusion in acute myocardial infarction. / Muller, Olivier; Delrue, Leen; Hamilos, Michalis; Vercauteren, Steven; Ntalianis, Argyrios; Trana, Catalina; Mangiacapra, Fabio; Dierickx, Karen; De Bruyne, Bernard; Wijns, William; Behfar, Atta; Barbato, Emanuele; Terzic, Andre; Vanderheyden, Marc; Bartunek, Jozef.

In: EuroIntervention, Vol. 7, No. 4, 08.2011, p. 458-466.

Research output: Contribution to journalArticle

Muller, O, Delrue, L, Hamilos, M, Vercauteren, S, Ntalianis, A, Trana, C, Mangiacapra, F, Dierickx, K, De Bruyne, B, Wijns, W, Behfar, A, Barbato, E, Terzic, A, Vanderheyden, M & Bartunek, J 2011, 'Transcriptional fingerprint of human whole blood at the site of coronary occlusion in acute myocardial infarction', EuroIntervention, vol. 7, no. 4, pp. 458-466. https://doi.org/10.4244/EIJV7I4A75
Muller, Olivier ; Delrue, Leen ; Hamilos, Michalis ; Vercauteren, Steven ; Ntalianis, Argyrios ; Trana, Catalina ; Mangiacapra, Fabio ; Dierickx, Karen ; De Bruyne, Bernard ; Wijns, William ; Behfar, Atta ; Barbato, Emanuele ; Terzic, Andre ; Vanderheyden, Marc ; Bartunek, Jozef. / Transcriptional fingerprint of human whole blood at the site of coronary occlusion in acute myocardial infarction. In: EuroIntervention. 2011 ; Vol. 7, No. 4. pp. 458-466.
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AU - Delrue, Leen

AU - Hamilos, Michalis

AU - Vercauteren, Steven

AU - Ntalianis, Argyrios

AU - Trana, Catalina

AU - Mangiacapra, Fabio

AU - Dierickx, Karen

AU - De Bruyne, Bernard

AU - Wijns, William

AU - Behfar, Atta

AU - Barbato, Emanuele

AU - Terzic, Andre

AU - Vanderheyden, Marc

AU - Bartunek, Jozef

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N2 - Aims: Transcriptome patterns associated with acute myocardial infarction at the site of coronary occlusion are largely unknown. The aim of this study was to decipher the angiogenic, atherosclerotic, and inflammatory mRNA profiles in whole blood samples collected at the site of coronary occlusion in patients with ST-elevation myocardial infarction (STEMI). Methods and results: In five consecutive patients with STEMI, blood was sampled at the site of occlusion (local) and in the systemic circulation (peripheral) during primary percutaneous coronary intervention. RNA was extracted from whole blood samples. Among 221 genes involved in angiogenesis, inflammation and atherosclerosis, 24 were shown to be differentially modulated locally, by analysis with custom-designed DNA array technology. Validation in 28 distinct STEMI patients using real-time quantitative PCR identified seven out of these 24 genes to be consistently and significantly upregulated in local versus peripheral blood (p<0.05). Three genes were chemokine family members (CCL2, CCL18 and CXCL12), three genes belonged to the cell-cell and cell-extracellular matrix family (FN1, CDH5 and SPP1), and one gene was representative of the lipoprotein family (APOE). Conclusions: We identified a set of whole blood transcripts induced at the site of coronary occlusion in the acute phase of myocardial infarction. Resolved genes indicate a predominant role for chemokines, cell-extracellular matrix, and lipoprotein alterations in the pathophysiology of acute myocardial infarction and the initial response to myocardial injury.

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