Signal transduction of a tissue interaction during embryonic heart development.

摘要: During early cardiac development, progenitors of the valves and septa heart are formed by an epithelial-mesenchymal cell transformation endothelial cells atrioventricular (AV) canal. We have previously shown that this event is due to interaction between endothelium products myocardium found within extracellular matrix. The present study examines signal transduction mechanisms governing differentiation AV canal endothelium. Activators protein kinase C (PKC), phorbol myristate acetate (PMA) mezerein, both produced incomplete phenotypic in vitro bioassay for transformation. On other hand, inhibitors PKC (H-7 staurosporine) tyrosine (genistein) blocked cellular response native or a myocardially-conditioned medium. Intracellular free calcium concentration ([Ca2+]i) was measured single microscopic digital analysis fura 2 fluorescence. Addition myocardial conditioned medium containing transforming stimulus specific increase [Ca2+]i "competent" canal, but not ventricular, cells. Epithelial-mesenchymal inhibited pertussis toxin cholera toxin. These data lead hypothesis tissue mediated G one more activities. In receptor activation, competent demonstrate [Ca2+]i. Together, provide direct evidence regional temporal regulation processes which mediate matrix-mediated embryo.