Editors' ChoiceHeart Disease

The Bone Marrow: Friend or Foe of the Heart?

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Science Translational Medicine  15 Aug 2012:
Vol. 4, Issue 147, pp. 147ec147
DOI: 10.1126/scitranslmed.3004725

Every day, the bone marrow produces billions of cells. Hematopoietic stem cells (HSC) are rare but can make any type of blood cell. The idea to harness their pluripotency to repair failing hearts has created excitement in the cardiovascular community. As an interesting by-product of a trial assessing tissue regeneration with bone marrow cells in patients after myocardial infarction (MI), Assmus and colleagues provided new insight into basic immunology of atherosclerosis.

Assmus et al. imaged the bone marrow in 41 patients 7 days after MI with [18F]fluorodeoxyglucose-positron emission tomography (18FDG PET). The imaging signal in the bone marrow was higher compared with those of 15 control patients, reflecting accentuated glucose uptake after MI. Flow cytometric analysis of bone marrow aspirates 2 to 8 days after MI showed an increased frequency of HSC, suggesting elevated hematopoietic activity. The clinical data were supplemented with preclinical findings: After coronary ligation in mice, the authors found HSC release into circulation and a higher proliferative capacity of the bone marrow. Most likely, these findings reflect the hematopoietic system's response to ischemic injury. The infarct recruits millions of leukocytes, cells that arise from HSC in the bone marrow and the spleen. Importantly, these very same leukocytes (i.e., monocytes and macrophages) are the driving force behind the growth of atherosclerotic lesions. Thus, the increased activity of the bone marrow after MI may lead to a higher systemic supply of immune cells.

The PET 18FDG signal increase is nonspecific, because we do not know which cells in the bone marrow take up more glucose and why. However, in conjunction with the cellular analyses, Assmus and coauthors make a compelling argument that the bone marrow activity increases after MI, to release progenitors and leukocytes. These cells may repair the heart but could also destabilize the next atherosclerotic plaque prone to rupture, at a time when many patients have their second or third MI. The reaction of the hematopoietic system to MI may help healing the heart or may be harmful, so we should keep a close eye on the bone marrow when dealing with coronary heart disease and its complications.

B. Assmus et al., Acute myocardial infarction activates progenitor cells and increases Wnt signalling in the bone marrow. Eur. Heart J. 33, 1911–1919 (2012). [PubMed]

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