期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 90, 期 -, 页码 120-128出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2015.12.007
关键词
Bone marrow transplantation; Macrophage polarisation; Myocardial infarction
资金
- British Heart Foundation [RG/13/11/30384]
- Fondation Leducq Transatlantic Network of Excellence
- Department of Health via a National Institute for Health Research (NIHR) Biomedical Research Centre award
- King's College London
- King's College Hospital NHS Foundation Trust
- British Heart Foundation [RG/13/11/30384] Funding Source: researchfish
Background: Bone marrow transplantation (BMT) is commonly used in experimental studies to investigate the contribution of BM-derived circulating cells to different disease processes. During studies investigating the cardiac response to acute myocardial infarction (MI) induced by permanent coronary ligation in mice that had previously undergone BMT, we found that BMT itself affects the remodelling response. Methods and results: Compared to matched naive mice, animals that had previously undergone BMT developed significantly less post-MI adverse remodelling, infarct thinning and contractile dysfunction as assessed by serial magnetic resonance imaging. Cardiac rupture in male mice was prevented. Histological analysis showed that the infarcts of mice that had undergone BMT had a significantly higher number of inflammatory cells, surviving cardiomyocytes and neovessels than control mice, as well as evidence of significant haemosiderin deposition. Flow cytometric and histological analyses demonstrated a higher number of alternatively activated (M2) macrophages in myocardium of the BMT group compared to control animals even before MI, and this increased further in the infarcts of the BMT mice after MI. Conclusions: The process of BMT itself substantially alters tissue macrophage phenotype and the subsequent response to acute MI. An increase in alternatively activated macrophages in this setting appears to enhance cardiac recovery after MI. (C) 2015 The Authors. Published by Elsevier Ltd.
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