Abstract
Intercellular communication (IC) mediated by gap junctions (gj) occurs during embryonal development and appears to be important for normal differentiation through the exchange of morphogenetic signalling substances. Disruption of IC by chemicals may induce abnormal development resulting from failed cell-cell interactions. It was established in the present study that genotypically normal human embryonal palate mesenchyme (HEPM) cells displayed IC in cell culture and that the transfer of [3H]uridine nucleotides was inhibited by the potent embryotoxin and teratogen 12-O-tetradecanoyl-phorbol-13-acetate (TPA). IC was mediated by gj which were revealed by freeze-fracture and electron microscopy. Quantitative morphometric analysis showed that inhibition of IC by TPA coincided with a significant reduction in the number of gj. The observations suggest that inhibition of IC by the teratogen TPA may be one among the many mechanisms believed to be responsible for the induction of abnormal development by chemical teratogens.
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