Cardiomyocytes overexpressing TNF-alpha attract migration of embryonic stem cells via activation of p38 and c-Jun amino-terminal kinase.

نویسندگان

  • Yu Chen
  • Qingen Ke
  • Yinke Yang
  • Jamal S Rana
  • Jian Tang
  • James P Morgan
  • Yong-Fu Xiao
چکیده

Tumor necrosis factor-alpha (TNF-alpha) plays an important role in the pathogenesis of myocardial infarction. Stem cells are able to regenerate infarcted myocardium. This study investigated whether TNF-alpha 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-alpha cDNA, were plated in the lower compartments and mouse ESCs tagged with green fluorescent protein were added to the upper compartments. TNF-alpha level was significantly increased in the medium of the lower compartments seeded with TNF-alpha-transfected cardiomyocytes. Compared with the controls, overexpression of TNF-alpha 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-alpha receptor (TNF-RII), but not by the antibody against the type I TNF-alpha 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-alpha-treated ESCs. Inhibition of the activity of p38 or JNK significantly attenuated TNF-alpha-induced ESC migration. Our data demonstrate that excessive TNF-alpha stimulates TNF-RII and enhances migration of ESCs in vitro. Activation of p38 and JNK is required for TNF-alpha-enhanced ESC migration.

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عنوان ژورنال:
  • FASEB journal : official publication of the Federation of American Societies for Experimental Biology

دوره 17 15  شماره 

صفحات  -

تاریخ انتشار 2003