Cell surface galactosyltransferase acts as a general modulator of rat acinar cell proliferation

Publisher Website
Google Scholar
Abstract
Several physiological parameters were examined for inducing acinar cell proliferation and corresponding increased expression of β1–4 galactosyltransferase. In this study, dietary changes causing acinar cell proliferation included the following: the introduction of animals to a liquid diet (causing gland atrophy) followed by reintroduction of solid chow, gustatory stimulation provided by the introduction of 0.5% citric acid to animal drinking water, and removal of the submandibular gland with subsequent reliance on the parotid gland for salivary protein. Alterations in growth factor levels were produced by injecting animals with a chronic (3 day) regimen of either nerve growth factor or epidermal growth factor. Parotid gland proliferation could be blocked in all cases except EGF by the injection of propranolol, a β-adrenoceptor antagonist, or the galactosyltransferase specific modifier protein, α-lactalbumin. EGF-induced proliferation could, however, be prevented by treating the animals with monoclonal antibody to EGF receptor or galactosyltransferase modifier protein a-lactalbumin. These results for normal acinar cell proliferation suggest a direct role for cell surface β1–4 galactosyltransferase in signalling and maintaining active cell growth.