Acute myocardial infarction activates distinct inflammation and proliferation pathways in circulating monocytes, prior to recruitment, and identified through conserved transcriptional responses in mice and humans
Monocytes play critical roles in tissue injury and repair following acute myocardial infarction (AMI). Specifically targeting inflammatory monocytes in experimental models leads to reduced infarct size and improved healing. However, data from humans are sparse, and it remains unclear whether monocyt...
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| Published in: | European heart journal Vol. 36; no. 29; p. 1923 |
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| Main Authors: | , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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01.08.2015
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| ISSN: | 1522-9645, 1522-9645 |
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| Abstract | Monocytes play critical roles in tissue injury and repair following acute myocardial infarction (AMI). Specifically targeting inflammatory monocytes in experimental models leads to reduced infarct size and improved healing. However, data from humans are sparse, and it remains unclear whether monocytes play an equally important role in humans. The aim of this study was to investigate whether the monocyte response following AMI is conserved between humans and mice and interrogate patterns of gene expression to identify regulated functions.
Thirty patients (AMI) and 24 control patients (stable coronary atherosclerosis) were enrolled. Female C57BL/6J mice (n = 6/group) underwent AMI by surgical coronary ligation. Myocardial injury was quantified by magnetic resonance imaging (human) and echocardiography (mice). Peripheral monocytes were isolated at presentation and at 48 h. RNA from separated monocytes was hybridized to Illumina beadchips. Acute myocardial infarction resulted in a significant peripheral monocytosis in both species that positively correlated with the extent of myocardial injury. Analysis of the monocyte transcriptome following AMI demonstrated significant conservation and identified inflammation and mitosis as central processes to this response. These findings were validated in both species.
Our findings show that the monocyte transcriptome is conserved between mice and humans following AMI. Patterns of gene expression associated with inflammation and proliferation appear to be switched on prior to their infiltration of injured myocardium suggesting that the specific targeting of inflammatory and proliferative processes in these immune cells in humans are possible therapeutic strategies. Importantly, they could be effective in the hours after AMI. |
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| AbstractList | Monocytes play critical roles in tissue injury and repair following acute myocardial infarction (AMI). Specifically targeting inflammatory monocytes in experimental models leads to reduced infarct size and improved healing. However, data from humans are sparse, and it remains unclear whether monocytes play an equally important role in humans. The aim of this study was to investigate whether the monocyte response following AMI is conserved between humans and mice and interrogate patterns of gene expression to identify regulated functions.AIMSMonocytes play critical roles in tissue injury and repair following acute myocardial infarction (AMI). Specifically targeting inflammatory monocytes in experimental models leads to reduced infarct size and improved healing. However, data from humans are sparse, and it remains unclear whether monocytes play an equally important role in humans. The aim of this study was to investigate whether the monocyte response following AMI is conserved between humans and mice and interrogate patterns of gene expression to identify regulated functions.Thirty patients (AMI) and 24 control patients (stable coronary atherosclerosis) were enrolled. Female C57BL/6J mice (n = 6/group) underwent AMI by surgical coronary ligation. Myocardial injury was quantified by magnetic resonance imaging (human) and echocardiography (mice). Peripheral monocytes were isolated at presentation and at 48 h. RNA from separated monocytes was hybridized to Illumina beadchips. Acute myocardial infarction resulted in a significant peripheral monocytosis in both species that positively correlated with the extent of myocardial injury. Analysis of the monocyte transcriptome following AMI demonstrated significant conservation and identified inflammation and mitosis as central processes to this response. These findings were validated in both species.METHODS AND RESULTSThirty patients (AMI) and 24 control patients (stable coronary atherosclerosis) were enrolled. Female C57BL/6J mice (n = 6/group) underwent AMI by surgical coronary ligation. Myocardial injury was quantified by magnetic resonance imaging (human) and echocardiography (mice). Peripheral monocytes were isolated at presentation and at 48 h. RNA from separated monocytes was hybridized to Illumina beadchips. Acute myocardial infarction resulted in a significant peripheral monocytosis in both species that positively correlated with the extent of myocardial injury. Analysis of the monocyte transcriptome following AMI demonstrated significant conservation and identified inflammation and mitosis as central processes to this response. These findings were validated in both species.Our findings show that the monocyte transcriptome is conserved between mice and humans following AMI. Patterns of gene expression associated with inflammation and proliferation appear to be switched on prior to their infiltration of injured myocardium suggesting that the specific targeting of inflammatory and proliferative processes in these immune cells in humans are possible therapeutic strategies. Importantly, they could be effective in the hours after AMI.CONCLUSIONSOur findings show that the monocyte transcriptome is conserved between mice and humans following AMI. Patterns of gene expression associated with inflammation and proliferation appear to be switched on prior to their infiltration of injured myocardium suggesting that the specific targeting of inflammatory and proliferative processes in these immune cells in humans are possible therapeutic strategies. Importantly, they could be effective in the hours after AMI. Monocytes play critical roles in tissue injury and repair following acute myocardial infarction (AMI). Specifically targeting inflammatory monocytes in experimental models leads to reduced infarct size and improved healing. However, data from humans are sparse, and it remains unclear whether monocytes play an equally important role in humans. The aim of this study was to investigate whether the monocyte response following AMI is conserved between humans and mice and interrogate patterns of gene expression to identify regulated functions. Thirty patients (AMI) and 24 control patients (stable coronary atherosclerosis) were enrolled. Female C57BL/6J mice (n = 6/group) underwent AMI by surgical coronary ligation. Myocardial injury was quantified by magnetic resonance imaging (human) and echocardiography (mice). Peripheral monocytes were isolated at presentation and at 48 h. RNA from separated monocytes was hybridized to Illumina beadchips. Acute myocardial infarction resulted in a significant peripheral monocytosis in both species that positively correlated with the extent of myocardial injury. Analysis of the monocyte transcriptome following AMI demonstrated significant conservation and identified inflammation and mitosis as central processes to this response. These findings were validated in both species. Our findings show that the monocyte transcriptome is conserved between mice and humans following AMI. Patterns of gene expression associated with inflammation and proliferation appear to be switched on prior to their infiltration of injured myocardium suggesting that the specific targeting of inflammatory and proliferative processes in these immune cells in humans are possible therapeutic strategies. Importantly, they could be effective in the hours after AMI. |
| Author | Godec, Jernej Choudhury, Robin P Digby, Janet E Channon, Keith M Ruparelia, Neil Dall'Armellina, Erica Neubauer, Stefan Kharbanda, Rajesh K Banning, Adrian P Lee, Regent Lygate, Craig A Chai, Joshua T Forfar, J Colin McAndrew, Debra Prendergast, Bernard D Haining, Nicholas W |
| Author_xml | – sequence: 1 givenname: Neil surname: Ruparelia fullname: Ruparelia, Neil organization: Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK Oxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK – sequence: 2 givenname: Jernej surname: Godec fullname: Godec, Jernej organization: Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA – sequence: 3 givenname: Regent surname: Lee fullname: Lee, Regent organization: Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK – sequence: 4 givenname: Joshua T surname: Chai fullname: Chai, Joshua T organization: Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK – sequence: 5 givenname: Erica surname: Dall'Armellina fullname: Dall'Armellina, Erica organization: Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK Acute Vascular Imaging Centre, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK – sequence: 6 givenname: Debra surname: McAndrew fullname: McAndrew, Debra organization: Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK – sequence: 7 givenname: Janet E surname: Digby fullname: Digby, Janet E organization: Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK – sequence: 8 givenname: J Colin surname: Forfar fullname: Forfar, J Colin organization: Oxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK – sequence: 9 givenname: Bernard D surname: Prendergast fullname: Prendergast, Bernard D organization: Oxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK – sequence: 10 givenname: Rajesh K surname: Kharbanda fullname: Kharbanda, Rajesh K organization: Oxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK – sequence: 11 givenname: Adrian P surname: Banning fullname: Banning, Adrian P organization: Oxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK – sequence: 12 givenname: Stefan surname: Neubauer fullname: Neubauer, Stefan organization: Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK – sequence: 13 givenname: Craig A surname: Lygate fullname: Lygate, Craig A organization: Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK – sequence: 14 givenname: Keith M surname: Channon fullname: Channon, Keith M organization: Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK Oxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK – sequence: 15 givenname: Nicholas W surname: Haining fullname: Haining, Nicholas W organization: Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA – sequence: 16 givenname: Robin P surname: Choudhury fullname: Choudhury, Robin P email: robin.choudhury@cardiov.ox.ac.uk organization: Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK Oxford Heart Centre, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK Acute Vascular Imaging Centre, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK robin.choudhury@cardiov.ox.ac.uk |
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| Copyright | The Author 2015. Published by Oxford University Press on behalf of the European Society of Cardiology. |
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| Keywords | Monocytes Inflammation Acute myocardial infarction Mitosis Genomics |
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| SubjectTerms | Aged Animals Case-Control Studies Cell Proliferation - physiology Female Gene Expression Profiling Humans Inflammation - immunology Inflammation - pathology Leukocytes, Mononuclear - immunology Leukocytes, Mononuclear - pathology Ligation Magnetic Resonance Angiography Male Mice, Inbred C57BL Middle Aged Myocardial Infarction - genetics Myocardial Infarction - immunology Myocardial Infarction - pathology Phenotype Transcription, Genetic - genetics Transcription, Genetic - immunology Transcriptional Activation - physiology |
| Title | Acute myocardial infarction activates distinct inflammation and proliferation pathways in circulating monocytes, prior to recruitment, and identified through conserved transcriptional responses in mice and humans |
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