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Myocardial production and release of MCP-1 and SDF-1 following myocardial infarction: differences between mice and man

Andrew J Boyle1*, Yerem Yeghiazarians1, Henry Shih1, Joy Hwang1, Jianqin Ye1, Rich Sievers1, Daiwei Zheng1, Jath Palasubramaniam2, Dharshan Palasubramaniam2, Connie Karschimkus2, Robert Whitbourn2, Alicia Jenkins2 and Andrew M Wilson2

Author Affiliations

1 Department of Medicine, Division of Cardiology, University of California San Francisco, San Francisco USA

2 St Vincent's Hospital Department of Medicine, University of Melbourne, Melbourne Australia

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Journal of Translational Medicine 2011, 9:150  doi:10.1186/1479-5876-9-150

Published: 12 September 2011



Stem cell homing to the heart is mediated by the release of chemo-attractant cytokines. Stromal derived factor -1 alpha (SDF-1a) and monocyte chemotactic factor 1(MCP-1) are detectable in peripheral blood after myocardial infarction (MI). It remains unknown if they are produced by, and released from, the heart in order to attract stem cells to repair the damaged myocardium.


Murine hearts were studied for expression of MCP-1 and SDF-1a at day 3 and day 28 following myocardial infarction to determine whether production is increased following MI. In addition, we studied the coronary artery and coronary sinus (venous) blood from patients with normal coronary arteries, stable coronary artery disease (CAD), unstable angina and MI to determine whether these cytokines are released from the heart into the systemic circulation following MI.


Both MCP-1 and SDF-1a are constitutively produced and released by the heart. MCP-1 mRNA is upregulated following murine experimental MI, but SDF-1a is suppressed. There is less release of SDF-1a into the systemic circulation in patients with all stages of CAD including MI, mimicking the animal model. However MCP-1 release from the human heart following MI is also suppressed, which is the exact opposite of the animal model.


SDF-1a and MCP-1 release from the human heart are suppressed following MI. In the case of SDF-1a, the animal model appropriately reflects the human situation. However, for MCP-1 the animal model is the exact opposite of the human condition. Human observational studies like this one are paramount in guiding translation from experimental studies to clinical trials.