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 inJournal of the American Heart Association Vol. 3; no. 3; pp. e000839 - n/a
Main Authors Nagai, Toshiyuki, Honda, Satoshi, Sugano, Yasuo, Matsuyama, Taka‐aki, Ohta‐Ogo, Keiko, Asaumi, Yasuhide, Ikeda, Yoshihiko, Kusano, Kengo, Ishihara, Masaharu, Yasuda, Satoshi, Ogawa, Hisao, Ishibashi‐Ueda, Hatsue, Anzai, Toshihisa
Format Journal Article
LanguageEnglish
Published England Blackwell Publishing Ltd 03.06.2014
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ISSN2047-9980
2047-9980
DOI10.1161/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.
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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Issue 3
Keywords cardiac rupture
inflammation
reparative fibrosis
dendritic cell
myocardial infarction
Language English
License Attribution-NonCommercial
2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
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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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proquest
pubmed
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Index Database
Enrichment Source
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StartPage e000839
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
URI https://onlinelibrary.wiley.com/doi/abs/10.1161%2FJAHA.114.000839
https://www.ncbi.nlm.nih.gov/pubmed/24895162
https://www.proquest.com/docview/1532949027
https://pubmed.ncbi.nlm.nih.gov/PMC4309075
Volume 3
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