Abstract
Nerve growth factor (NGF) has previously been shown to increase the rate of adhesion of PC‐12 pheochromocytoma cells to cell culture dishes. This increase in the rate of adhesion was postulated to be important in NGF‐mediated neurite outgrowth. We now report that epidermal growth factor (EGF) is also able to increase the rate of adhesion of PC‐12 cells to cell culture dishes, but does not elicit neurite outgrowth. The dose‐response curve for EGF is bell‐shaped, in contrast to the more classically shaped dose‐response curve obtained with NGF.
Tetradecanoyl‐phorbol‐acetate (TPA), a potent tumor promoter, blocks the EGF‐induced increase in adhesion rate of PC‐12 cells, but does not alter the NGF‐induced increase in adhesion rate. TPA shifts the EGF binding curve to the right for PC‐12 cells, but does not alter maximal EGF binding at saturating concentrations of EGF. The binding of NGF to PC‐12 cells is not affected by TPA. NGF‐induced neurite formation by PC‐12 cells is unaffected by TPA, in contrast to the previously reported delay of neurite outgrowth of serum‐deprived neuroblastoma cells and NGF‐exposed chick embryonic ganglia cells.
NGF and EGF both cause a decrease in the number of short microvilli and an increase in the number of long microvilli on PC‐12 cells. TPA blocks the decrease in the number of short microvilli in EGF‐treated cells, but not in NGF‐treated cells. Long microvilli formation is blocked by TPA in both conditions, suggesting the latter are not involved in the increased adhesion rates.