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J Mol Cell Cardiol. 2016 Jan;90:120-8. doi: 10.1016/j.yjmcc.2015.12.007. Epub 2015 Dec 11.

Bone marrow transplantation modulates tissue macrophage phenotype and enhances cardiac recovery after subsequent acute myocardial infarction.

Author information

1
Cardiovascular Division, King's College London British Heart Foundation Centre of Excellence, London, UK; Division of Imaging Sciences and Bioengineering, King's College London British Heart Foundation Centre of Excellence, London, UK.
2
Cardiovascular Division, King's College London British Heart Foundation Centre of Excellence, London, UK.
3
BHF/University Centre for Cardiovascular Science, University of Edinburgh, Queens Medical Research Institute, Edinburgh, UK.
4
Cardiovascular Division, King's College London British Heart Foundation Centre of Excellence, London, UK; Department of Cardiology, Universitätsklinikum Regensburg, Germany.
5
Department of Cardiology, Universitätsklinikum Regensburg, Germany.
6
Division of Imaging Sciences and Bioengineering, King's College London British Heart Foundation Centre of Excellence, London, UK.
7
Department of Histopathology, King's College Hospital, London, UK.
8
Cardiovascular Division, King's College London British Heart Foundation Centre of Excellence, London, UK. Electronic address: ajay.shah@kcl.ac.uk.

Abstract

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.

KEYWORDS:

Bone marrow transplantation; Macrophage polarisation; Myocardial infarction

PMID:
26688473
PMCID:
PMC4727788
DOI:
10.1016/j.yjmcc.2015.12.007
[Indexed for MEDLINE]
Free PMC Article

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