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MBC in Press, published online ahead of print May 16, 2007
Mol. Biol. Cell 10.1091/mbc.E07-02-0166

A more recent version of this article appeared on August 1, 2007
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Submitted on February 23, 2007
Revised on April 23, 2007
Accepted on May 8, 2007

Mesenchymal Stem Cells Utilize Integrin {beta}1 Not CXCR4 for Myocardial Migration and Engraftment

James E. Ip,* Yaojiong Wu,* Jing Huang, Lunan Zhang, Richard E. Pratt, and Victor J. Dzau

Department of Medicine, Duke University School of Medicine, Durham, NC 27710, and Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115

Monitoring Editor: Richard Assoian

Recent evidence have demonstrated the importance of bone marrow derived mesenchymal stem cells (BM-MSCs) in the repair of damaged myocardium. The molecular mechanisms of engraftment and migration of BM-MSC in the ischemic myocardium are unknown. In this study, we developed a functional genomics approach toward the identification of mediators of engraftment and migration of BM-MSC within the ischemic myocardium. Our strategy involves microarry profiling (>22000 probes) of ischemic hearts, complemented by RT-PCR and FACS of corresponding adhesion molecule and cytokine receptors in BM-MSCs to focus on the coexpressed pairs only. Our data revealed 9 complementary adhesion molecules and cytokine receptors, including integrin {beta}1, integrin {alpha}4, and CXCR4. To examine their functional contributions, we first blocked selectively these receptors by pre-incubation of BM-MSCs with specific neutralizing antibodies, then administered these cells intramyocardially. A significant reduction in the total number of BM-MSC in the infarcted myocardium was observed after integrin {beta}1 blockade, but not integrin {alpha}4 or CXCR4 blockade. The latter observation is distinctively different from that reported for hematopoietic stem cells (HSC). Thus, our data show that BM-MSCs utilize a different pathway from HSCs for intramyocardial trafficking and engraftment.

*These authors contributed equally to this work.

Address correspondence to: Victor J. Dzau (victor.dzau{at}duke.edu)




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