12-O-TETRADECANOYLPHORBOL-13-ACETATE-INDUCED INHIBITION OF GAP JUNCTIONAL COMMUNICATION IS DIFFERENTIALLY REGULATED IN A TRANSFORMATION-SENSITIVE SYRIAN-HAMSTER EMBRYO CELL-LINE COMPARED TO EARLY-PASSAGE SHE CELLS

The transformation-sensitive cell-line BPNi was more susceptible to 12 -O-tetradecanoylphorbol-13-acetate (TPA)-induced inhibition of gap jun ctional intercellular communication (GJIC) than early passage Syrian h amster embryo (SHE) cells, while the potency of TPA to down-regulate E GF-binding was similar in the two cell types. The kinetics of TPA-indu ced inhibition of GJIC suggested that different mechanisms may operate at high and low TPA concentrations. The initial inhibition after expo sure to high TPA concentrations was followed by a recovery of GJIC. Th e recovery was much more pronounced in SHE than in BPNi cells. This ef fect could not be explained by differences in down-regulation of prote in kinase C. Removal of high TPA concentrations also resulted in a fas ter recovery of GJIC in SHE than in BPNi cells. In addition, although forskolin induced a similar protection against the inhibitory effect o f TPA on GJIC, forskolin restored GJIC blocked by TPA much faster in S HE than in BPNi cells. Thus, BPNi cells are more sensitive to TPA indu ced inhibition of GJIC than SHE cells, and have reduced capability to recover from down-regulated GJIC as compared to SHE cells.