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Am J Physiol Heart Circ Physiol (May 12, 2006). doi:10.1152/ajpheart.00363.2005
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Submitted on April 12, 2005
Accepted on May 3, 2006

Vascular Endothelial Growth Factor Promotes Cardiomyocyte Differentiation of Embryonic Stem Cells

Yu Chen1, Ivo Amende2, Thomas G Hampton2, Yinke Yang2, Qingen Ke2, Jiang-Yong Min2, Yong-Fu Xiao2, and James P. Morgan3

1 Cardiology, Beth Israel Deaconess MC, Harvard Medical School, Boston, Massachusetts, United States; Cell Biology, Memorial Sloan-Kettering Cancer Center, Boston, Massachusetts, United States
2 Cardiology, Beth Israel Deaconess MC, Harvard Medical School, Boston, Massachusetts, United States
3 Harvard Medical School, Beth Israel Deaconess medical Center, United States; Caritas St. Elizabeth's and Tufts Univ School Med, Boston, Massachusetts, United States

Embryonic stem cells (ESCs) overexpressing the vascular endothelial growth factor (VEGF) improve cardiac function in mouse models of myocardial ischemia and infarction by mechanisms that are poorly understood. Here we studied the effects of VEGF on cardiomyocyte differentiation of mouse ESCs in vitro. We used flow cytometry to determine the expression of {alpha}-myosin heavy chain ({alpha}-MHC), cardiac troponin I (cTn-I), and Nkx2.5 in differentiated ESCs. VEGF (20 ng/ml) significantly enhanced {alpha}-MHC, cTn-I and Nkx2.5 expression in differentiated ESCs. Western blot analysis confirmed these findings. We found that VEGF receptors Flt-1 and Flk-1 expression increased during ESC differentiation. Antibodies against Flk-1 totally blocked and against Flt-1 partially blocked VEGF-induced NKx2.5 positive stained cells. The ERK inhibitor, PD098059, abolished VEGF-induced cardiomyocyte differentiation of ESCs. Our results suggest that VEGF promotes cardiomyocyte differentiation predominantly by ERK-mediated Flk-1 activation and, to a lesser extent, by Flt-1 activation. These findings may be of significance for stem cell and growth factor therapies to regenerate failing cardiomyocytes.




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