Regulation of cell-surface galactosyltransferase in isoproterenol-treated mouse parotid glands.

Chronic injection of isoproterenol into mice resulted in hypertrophy and hyperplasia of the parotid gland. As previously described for the rat, cell proliferation was accompanied by an increase in total membrane-associated galactosyltransferase. A plasma membrane localization was determined by fluorescence-activated sorting of intact cells. Co-administration of the galactosyltransferase modifier protein, alpha-lactalbumin, or the calmodulin inhibitor, trifluoperazine, blocked acinar cell proliferation by 96 h post-treatment but not at 24 h. While alpha-lactalbumin appeared to interfere with galactosyltransferase-substrate interactions, trifluoperazine prevented the appearance of cell-surface enzyme in isoproterenol-treated animals.