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attract migration of embryonic stem cells via activation of p38 and c-Jun amino-terminal kinase
Stem Cells Research Laboratory, The Charles A. Dana Research Institute and Harvard-Thorndike Laboratory, Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
1Correspondence: Cardiovascular Division, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Ave., Boston, MA 02215, USA. E-mail: yxiao{at}caregroup.harvard.edu
Tumor necrosis factor-
(TNF-) plays an important role in the pathogenesis of myocardial infarction. Stem cells are able to regenerate infarcted myocardium. This study investigated whether TNF- was able to induce migration of embryonic stem cells (ESCs) in vitro. We used a Transwell assay in which neonatal rat cardiomyocytes, with or without transfection of TNF- cDNA, were plated in the lower compartments and mouse ESCs tagged with green fluorescent protein were added to the upper compartments. TNF- level was significantly increased in the medium of the lower compartments seeded with TNF--transfected cardiomyocytes. Compared with the controls, overexpression of TNF- significantly enhanced migration of ESCs to the lower compartments. This enhancement was attenuated by preincubation of ESCs with the antibody against the type II TNF- receptor (TNF-RII), but not by the antibody against the type I TNF- receptor (TNF-RI). Western blot analysis showed that the phosphorylated protein levels of p38 and c-Jun amino-terminal kinase (JNK) were significantly increased in TNF--treated ESCs. Inhibition of the activity of p38 or JNK significantly attenuated TNF--induced ESC migration. Our data demonstrate that excessive TNF- stimulates TNF-RII and enhances migration of ESCs in vitro. Activation of p38 and JNK is required for TNF--enhanced ESC migration.—Chen, Y., Ke, Q., Yang, Y., Rana, J. S., Tang, J., Morgan, J. P., Xiao, Y.-F. Cardiomyocytes overexpressing TNF- attract migration of embryonic stem cells via activation of p38 and c-Jun amino-terminal kinase.
Key Words: myocardial infarction • transfection • Transwell assay
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