Isoproterenol, a β-adrenergic receptor agonist, causes hypertrophy and hyperplasia of the rat parotid gland. The stimulation of parotid acinar cells to a growth phase is accompanied by a cell surface localization of the enzyme 4β-galactosyltransferase. Alpha-lactalbumin, a specific modifier protein for 4β-galactosyltransferase, when given subsequent to the initiation of isoproterenol treatment and the commencement of parotid enlargement, resulted in a termination of gland hypertrophy and DNA synthesis. Gland size did not, however, return to control levels with the continued injection of isoproterenol and alpha- lactalbumin. In contrast, the injection of alpha-lactalbumin in neonatal rats (7-14 days post-partum) stimulated parotid gland hypertrophy and DNA synthesis. This treatment also lead to the precocious expression of the major parotid gland salivary enzyme, amylase.
|Number of pages||8|
|Journal||Biochemical and biophysical research communications|
|Publication status||Published - Aug 31 1987|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology