Decreased Myocardial Dendritic Cells is Associated With Impaired Reparative Fibrosis and Development of Cardiac Rupture After Myocardial Infarction in Humans
Background Dendritic cells (DC) play pivotal roles in regulating the immune system and inflammatory response. We previously reported DC infiltration in the infarcted heart and its immunoprotective roles in the post‐infarction healing process after experimental myocardial infarction (MI). However, it...
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Published in | Journal of the American Heart Association Vol. 3; no. 3; pp. e000839 - n/a |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Blackwell Publishing Ltd
03.06.2014
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Subjects | |
Online Access | Get full text |
ISSN | 2047-9980 2047-9980 |
DOI | 10.1161/JAHA.114.000839 |
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Abstract | Background
Dendritic cells (DC) play pivotal roles in regulating the immune system and inflammatory response. We previously reported DC infiltration in the infarcted heart and its immunoprotective roles in the post‐infarction healing process after experimental myocardial infarction (MI). However, its clinical significance has not been determined.
Methods and Results
The degree of DC infiltration and its correlation with the post‐infarction healing process in the human infarcted heart were investigated in 24 autopsy subjects after ST‐elevation MI. Patients were divided into two groups according to the presence (n=13) or absence (n=11) of cardiac rupture. The numbers of infiltrated DC and macrophages and the extent of fibrosis in the infarcted area were examined. In the rupture group, CD68+ macrophage infiltration was increased and CD209+ DC, and CD11c+ DC infiltration and the extent of reparative fibrosis were decreased compared with the non‐rupture group, under matched baseline characteristics including the time from onset to death and use of revascularization. Furthermore, there was a significant positive correlation between the number of infiltrating CD209+ DC, and CD11c+ DC and the extent of reparative fibrosis.
Conclusions
Decreased number of DC in human‐infarcted myocardial tissue was associated with increased macrophage infiltration, impaired reparative fibrosis, and the development of cardiac rupture after MI. These findings suggest a protective role of DC in post‐MI inflammation and the subsequent healing process. |
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AbstractList | Dendritic cells (DC) play pivotal roles in regulating the immune system and inflammatory response. We previously reported DC infiltration in the infarcted heart and its immunoprotective roles in the post-infarction healing process after experimental myocardial infarction (MI). However, its clinical significance has not been determined.BACKGROUNDDendritic cells (DC) play pivotal roles in regulating the immune system and inflammatory response. We previously reported DC infiltration in the infarcted heart and its immunoprotective roles in the post-infarction healing process after experimental myocardial infarction (MI). However, its clinical significance has not been determined.The degree of DC infiltration and its correlation with the post-infarction healing process in the human infarcted heart were investigated in 24 autopsy subjects after ST-elevation MI. Patients were divided into two groups according to the presence (n=13) or absence (n=11) of cardiac rupture. The numbers of infiltrated DC and macrophages and the extent of fibrosis in the infarcted area were examined. In the rupture group, CD68(+) macrophage infiltration was increased and CD209(+) DC, and CD11c(+) DC infiltration and the extent of reparative fibrosis were decreased compared with the non-rupture group, under matched baseline characteristics including the time from onset to death and use of revascularization. Furthermore, there was a significant positive correlation between the number of infiltrating CD209(+) DC, and CD11c(+) DC and the extent of reparative fibrosis.METHODS AND RESULTSThe degree of DC infiltration and its correlation with the post-infarction healing process in the human infarcted heart were investigated in 24 autopsy subjects after ST-elevation MI. Patients were divided into two groups according to the presence (n=13) or absence (n=11) of cardiac rupture. The numbers of infiltrated DC and macrophages and the extent of fibrosis in the infarcted area were examined. In the rupture group, CD68(+) macrophage infiltration was increased and CD209(+) DC, and CD11c(+) DC infiltration and the extent of reparative fibrosis were decreased compared with the non-rupture group, under matched baseline characteristics including the time from onset to death and use of revascularization. Furthermore, there was a significant positive correlation between the number of infiltrating CD209(+) DC, and CD11c(+) DC and the extent of reparative fibrosis.Decreased number of DC in human-infarcted myocardial tissue was associated with increased macrophage infiltration, impaired reparative fibrosis, and the development of cardiac rupture after MI. These findings suggest a protective role of DC in post-MI inflammation and the subsequent healing process.CONCLUSIONSDecreased number of DC in human-infarcted myocardial tissue was associated with increased macrophage infiltration, impaired reparative fibrosis, and the development of cardiac rupture after MI. These findings suggest a protective role of DC in post-MI inflammation and the subsequent healing process. Background Dendritic cells (DC) play pivotal roles in regulating the immune system and inflammatory response. We previously reported DC infiltration in the infarcted heart and its immunoprotective roles in the post‐infarction healing process after experimental myocardial infarction (MI). However, its clinical significance has not been determined. Methods and Results The degree of DC infiltration and its correlation with the post‐infarction healing process in the human infarcted heart were investigated in 24 autopsy subjects after ST‐elevation MI. Patients were divided into two groups according to the presence (n=13) or absence (n=11) of cardiac rupture. The numbers of infiltrated DC and macrophages and the extent of fibrosis in the infarcted area were examined. In the rupture group, CD68+ macrophage infiltration was increased and CD209+ DC, and CD11c+ DC infiltration and the extent of reparative fibrosis were decreased compared with the non‐rupture group, under matched baseline characteristics including the time from onset to death and use of revascularization. Furthermore, there was a significant positive correlation between the number of infiltrating CD209+ DC, and CD11c+ DC and the extent of reparative fibrosis. Conclusions Decreased number of DC in human‐infarcted myocardial tissue was associated with increased macrophage infiltration, impaired reparative fibrosis, and the development of cardiac rupture after MI. These findings suggest a protective role of DC in post‐MI inflammation and the subsequent healing process. Dendritic cells (DC) play pivotal roles in regulating the immune system and inflammatory response. We previously reported DC infiltration in the infarcted heart and its immunoprotective roles in the post-infarction healing process after experimental myocardial infarction (MI). However, its clinical significance has not been determined. The degree of DC infiltration and its correlation with the post-infarction healing process in the human infarcted heart were investigated in 24 autopsy subjects after ST-elevation MI. Patients were divided into two groups according to the presence (n=13) or absence (n=11) of cardiac rupture. The numbers of infiltrated DC and macrophages and the extent of fibrosis in the infarcted area were examined. In the rupture group, CD68(+) macrophage infiltration was increased and CD209(+) DC, and CD11c(+) DC infiltration and the extent of reparative fibrosis were decreased compared with the non-rupture group, under matched baseline characteristics including the time from onset to death and use of revascularization. Furthermore, there was a significant positive correlation between the number of infiltrating CD209(+) DC, and CD11c(+) DC and the extent of reparative fibrosis. Decreased number of DC in human-infarcted myocardial tissue was associated with increased macrophage infiltration, impaired reparative fibrosis, and the development of cardiac rupture after MI. These findings suggest a protective role of DC in post-MI inflammation and the subsequent healing process. |
Author | Yasuda, Satoshi Matsuyama, Taka‐aki Kusano, Kengo Ishibashi‐Ueda, Hatsue Asaumi, Yasuhide Ohta‐Ogo, Keiko Honda, Satoshi Anzai, Toshihisa Nagai, Toshiyuki Ishihara, Masaharu Ogawa, Hisao Sugano, Yasuo Ikeda, Yoshihiko |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24895162$$D View this record in MEDLINE/PubMed |
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Keywords | cardiac rupture inflammation reparative fibrosis dendritic cell myocardial infarction |
Language | English |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Dr Nagai and Dr Honda were equally contributed to the present study. |
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Snippet | Background
Dendritic cells (DC) play pivotal roles in regulating the immune system and inflammatory response. We previously reported DC infiltration in the... Dendritic cells (DC) play pivotal roles in regulating the immune system and inflammatory response. We previously reported DC infiltration in the infarcted... |
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SubjectTerms | Aged Antigens, CD - physiology Antigens, Differentiation, Myelomonocytic - physiology cardiac rupture Case-Control Studies Cell Adhesion Molecules - physiology dendritic cell Dendritic Cells - pathology Dendritic Cells - physiology Female Fibrosis Heart - physiopathology Heart Rupture, Post-Infarction - etiology Heart Rupture, Post-Infarction - pathology Heart Rupture, Post-Infarction - physiopathology Humans inflammation Lectins, C-Type - physiology Macrophages - pathology Macrophages - physiology Male myocardial infarction Myocardial Infarction - complications Myocardial Infarction - pathology Myocardial Infarction - physiopathology Myocardium - cytology Myocardium - pathology Original Research Receptors, Cell Surface - physiology reparative fibrosis |
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Title | Decreased Myocardial Dendritic Cells is Associated With Impaired Reparative Fibrosis and Development of Cardiac Rupture After Myocardial Infarction in Humans |
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