Alpha-lactalbumin acts as a bimodal regulator of rat parotid acinar cell growth

Michael G. Humphreys-Beher, Charlotte A. Schneyer, Tivadar Zelles

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)174-181
Number of pages8
JournalBiochemical and biophysical research communications
Volume147
Issue number1
DOIs
Publication statusPublished - Aug 31 1987

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ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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