Document Detail


Decreased Myocardial Dendritic Cells is Associated With Impaired Reparative Fibrosis and Development of Cardiac Rupture After Myocardial Infarction in Humans.
MedLine Citation:
PMID:  24895162     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
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.
Authors:
Toshiyuki Nagai; Satoshi Honda; Yasuo Sugano; Taka-Aki Matsuyama; Keiko Ohta-Ogo; Yasuhide Asaumi; Yoshihiko Ikeda; Kengo Kusano; Masaharu Ishihara; Satoshi Yasuda; Hisao Ogawa; Hatsue Ishibashi-Ueda; Toshihisa Anzai
Publication Detail:
Type:  Journal Article     Date:  2014-06-03
Journal Detail:
Title:  Journal of the American Heart Association     Volume:  3     ISSN:  2047-9980     ISO Abbreviation:  J Am Heart Assoc     Publication Date:  2014  
Date Detail:
Created Date:  2014-06-04     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101580524     Medline TA:  J Am Heart Assoc     Country:  England    
Other Details:
Languages:  eng     Pagination:  -     Citation Subset:  IM    
Copyright Information:
© 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Atrial fibrillation, stroke, and anticoagulation in medicare beneficiaries: trends by age, sex, and ...
Next Document:  Postextrasystolic blood pressure potentiation predicts poor outcome of cardiac patients.