Prasad K N, Carvalho E, Kumar S, Edwards-Prasad J, La Rosa F G
Center for Vitamins and Cancer Research, School of Medicine, University of Colorado Health Sciences Center, Denver 80262-0278.
Biochem Cell Biol. 1993 Jul-Aug;71(7-8):355-60. doi: 10.1139/o93-053.
Treatment of rats with isoproterenol (IPR, beta 1- and beta 2-agonist), dobutamine (beta 1-agonist), and terbutaline (beta 2-agonist) increased the cAMP level and cell proliferation, but it decreased alpha-amylase activity in parotid glands. Terbutaline was relatively less effective. Alpha-Amylase activity as determined by substrate hydrolysis was maximally depressed (85% of control) after 15 min of IPR treatment; however, alpha-amylase level as determined by Western immunoblotting with the primary antibody to alpha-amylase decreased maximally after 2 h of treatment. The level of alpha-amylase significantly decreased after 15 min of treatment, but the levels of alpha-amylase mRNAs of 702 and 1176 base pairs (bp) slightly increased at this time. This suggests that an increased rate of transcription or a decreased rate of degradation of alpha-amylase mRNAs without a proportional increase in the rate of translation of alpha-amylase occurs in parotid glands after treatment with IPR. The levels of alpha-amylase mRNAs decreased after 2 h of treatment; however, the level of alpha-mRNA of 702 bp continued to decline, but the level of alpha-mRNA of 1176 bp increased at 3 days after IPR treatment. The level of actin mRNA of 2200 bp increased at 15 min and remained elevated during the entire observation period. Results showed that IPR-induced elevation of cAMP increases cell proliferation, and alters the level and activity of alpha-amylase and the expression of alpha-amylase genes at different rates.
