Cell-surface galactosyltransferase acts as a modulator of rat and human acinar cell proliferation.

M. G. Humphreys-Beher, T. Zelles, N. Maeda, K. R. Purushotham, N. Cassisi, C. A. Schneyer

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Several physiological parameters were examined for inducing acinar cell proliferation and corresponding increased expression of beta 1-4 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 re-introduction 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 saliva protein and fluid. Alterations in growth factor levels were produced by injecting animals with a chronic (three-day) regimen of either nerve growth factor (NGF) or epidermal growth factor (EGF). In all cases of acinar cell proliferation in vivo, generated by the above treatments, cell-surface galactosyltransferase was detected along with the unique expression of a 4.5-kb proliferation-associated mRNA. Parotid gland proliferation could be blocked in all cases by the injection of the galactosyltransferase specific modifier protein, alpha-lactalbumin. Propranolol, a beta-adrenergic receptor antagonist, blocked proliferation in all cases except EGF treatment. EGF-induced proliferation could, however, be prevented if the animals were treated with monoclonal antibody to EGF receptor or with the galactosyltransferase modifier alpha-lactalbumin. As a comparison, human parotid tissue samples obtained from neoplastic pleomorphic adenomas, muco-epidermoid carcinoma, adenoid cystic carcinoma, and a bulimia patient were analyzed for galactosyltransferase expression by Northern blot of mRNA and plasma membrane isolation. Elevated levels of galactosyltransferase were found in all neoplastic tissue preparations as well as in the bulimia sample. Amylase synthesis was reduced in samples compared with surrounding normal tissue from the same patient. In vitro cell culturing of pleomorphic adenoma cells in the presence of galactosyltransferase modifier alpha-lactalbumin and substrate UDP-galactose inhibited proliferation in a dose-dependent fashion. Southern blot analysis of DNA from neoplastic parotid cells showed an alteration in chromosomal gene structure for the galactosyltransferase activator cDNA from the adenoid cystic carcinoma. These results for induced acinar cell proliferation as well as human neoplastic pathologies suggest a direct role for cell surface beta 1-4 galactosyltransferase in signaling growth. Furthermore, the proliferation-associated activity of galactosyltransferase suggests that it may be considered as a new type of cell growth regulator.

Original languageEnglish
Pages (from-to)45-60
Number of pages16
JournalAdvances in dental research
Volume4
Publication statusPublished - Jun 1990

Fingerprint

Galactosyltransferases
Acinar Cells
Cell Proliferation
Lactalbumin
N-Acetyllactosamine Synthase
Epidermal Growth Factor
Pleomorphic Adenoma
Adenoid Cystic Carcinoma
Bulimia
Parotid Gland
Uridine Diphosphate Galactose
Messenger RNA
Adrenergic Antagonists
Submandibular Gland
Receptors, Adrenergic, beta
Nerve Growth Factor
Amylases
Growth
Southern Blotting
Saliva

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Humphreys-Beher, M. G., Zelles, T., Maeda, N., Purushotham, K. R., Cassisi, N., & Schneyer, C. A. (1990). Cell-surface galactosyltransferase acts as a modulator of rat and human acinar cell proliferation. Advances in dental research, 4, 45-60.

Cell-surface galactosyltransferase acts as a modulator of rat and human acinar cell proliferation. / Humphreys-Beher, M. G.; Zelles, T.; Maeda, N.; Purushotham, K. R.; Cassisi, N.; Schneyer, C. A.

In: Advances in dental research, Vol. 4, 06.1990, p. 45-60.

Research output: Contribution to journalArticle

Humphreys-Beher, MG, Zelles, T, Maeda, N, Purushotham, KR, Cassisi, N & Schneyer, CA 1990, 'Cell-surface galactosyltransferase acts as a modulator of rat and human acinar cell proliferation.', Advances in dental research, vol. 4, pp. 45-60.
Humphreys-Beher, M. G. ; Zelles, T. ; Maeda, N. ; Purushotham, K. R. ; Cassisi, N. ; Schneyer, C. A. / Cell-surface galactosyltransferase acts as a modulator of rat and human acinar cell proliferation. In: Advances in dental research. 1990 ; Vol. 4. pp. 45-60.
@article{3486d6134df243e9af2423094f7e9f6f,
title = "Cell-surface galactosyltransferase acts as a modulator of rat and human acinar cell proliferation.",
abstract = "Several physiological parameters were examined for inducing acinar cell proliferation and corresponding increased expression of beta 1-4 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 re-introduction 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 saliva protein and fluid. Alterations in growth factor levels were produced by injecting animals with a chronic (three-day) regimen of either nerve growth factor (NGF) or epidermal growth factor (EGF). In all cases of acinar cell proliferation in vivo, generated by the above treatments, cell-surface galactosyltransferase was detected along with the unique expression of a 4.5-kb proliferation-associated mRNA. Parotid gland proliferation could be blocked in all cases by the injection of the galactosyltransferase specific modifier protein, alpha-lactalbumin. Propranolol, a beta-adrenergic receptor antagonist, blocked proliferation in all cases except EGF treatment. EGF-induced proliferation could, however, be prevented if the animals were treated with monoclonal antibody to EGF receptor or with the galactosyltransferase modifier alpha-lactalbumin. As a comparison, human parotid tissue samples obtained from neoplastic pleomorphic adenomas, muco-epidermoid carcinoma, adenoid cystic carcinoma, and a bulimia patient were analyzed for galactosyltransferase expression by Northern blot of mRNA and plasma membrane isolation. Elevated levels of galactosyltransferase were found in all neoplastic tissue preparations as well as in the bulimia sample. Amylase synthesis was reduced in samples compared with surrounding normal tissue from the same patient. In vitro cell culturing of pleomorphic adenoma cells in the presence of galactosyltransferase modifier alpha-lactalbumin and substrate UDP-galactose inhibited proliferation in a dose-dependent fashion. Southern blot analysis of DNA from neoplastic parotid cells showed an alteration in chromosomal gene structure for the galactosyltransferase activator cDNA from the adenoid cystic carcinoma. These results for induced acinar cell proliferation as well as human neoplastic pathologies suggest a direct role for cell surface beta 1-4 galactosyltransferase in signaling growth. Furthermore, the proliferation-associated activity of galactosyltransferase suggests that it may be considered as a new type of cell growth regulator.",
author = "Humphreys-Beher, {M. G.} and T. Zelles and N. Maeda and Purushotham, {K. R.} and N. Cassisi and Schneyer, {C. A.}",
year = "1990",
month = "6",
language = "English",
volume = "4",
pages = "45--60",
journal = "Advances in dental research",
issn = "0895-9374",
publisher = "International Association for Dental Research",

}

TY - JOUR

T1 - Cell-surface galactosyltransferase acts as a modulator of rat and human acinar cell proliferation.

AU - Humphreys-Beher, M. G.

AU - Zelles, T.

AU - Maeda, N.

AU - Purushotham, K. R.

AU - Cassisi, N.

AU - Schneyer, C. A.

PY - 1990/6

Y1 - 1990/6

N2 - Several physiological parameters were examined for inducing acinar cell proliferation and corresponding increased expression of beta 1-4 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 re-introduction 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 saliva protein and fluid. Alterations in growth factor levels were produced by injecting animals with a chronic (three-day) regimen of either nerve growth factor (NGF) or epidermal growth factor (EGF). In all cases of acinar cell proliferation in vivo, generated by the above treatments, cell-surface galactosyltransferase was detected along with the unique expression of a 4.5-kb proliferation-associated mRNA. Parotid gland proliferation could be blocked in all cases by the injection of the galactosyltransferase specific modifier protein, alpha-lactalbumin. Propranolol, a beta-adrenergic receptor antagonist, blocked proliferation in all cases except EGF treatment. EGF-induced proliferation could, however, be prevented if the animals were treated with monoclonal antibody to EGF receptor or with the galactosyltransferase modifier alpha-lactalbumin. As a comparison, human parotid tissue samples obtained from neoplastic pleomorphic adenomas, muco-epidermoid carcinoma, adenoid cystic carcinoma, and a bulimia patient were analyzed for galactosyltransferase expression by Northern blot of mRNA and plasma membrane isolation. Elevated levels of galactosyltransferase were found in all neoplastic tissue preparations as well as in the bulimia sample. Amylase synthesis was reduced in samples compared with surrounding normal tissue from the same patient. In vitro cell culturing of pleomorphic adenoma cells in the presence of galactosyltransferase modifier alpha-lactalbumin and substrate UDP-galactose inhibited proliferation in a dose-dependent fashion. Southern blot analysis of DNA from neoplastic parotid cells showed an alteration in chromosomal gene structure for the galactosyltransferase activator cDNA from the adenoid cystic carcinoma. These results for induced acinar cell proliferation as well as human neoplastic pathologies suggest a direct role for cell surface beta 1-4 galactosyltransferase in signaling growth. Furthermore, the proliferation-associated activity of galactosyltransferase suggests that it may be considered as a new type of cell growth regulator.

AB - Several physiological parameters were examined for inducing acinar cell proliferation and corresponding increased expression of beta 1-4 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 re-introduction 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 saliva protein and fluid. Alterations in growth factor levels were produced by injecting animals with a chronic (three-day) regimen of either nerve growth factor (NGF) or epidermal growth factor (EGF). In all cases of acinar cell proliferation in vivo, generated by the above treatments, cell-surface galactosyltransferase was detected along with the unique expression of a 4.5-kb proliferation-associated mRNA. Parotid gland proliferation could be blocked in all cases by the injection of the galactosyltransferase specific modifier protein, alpha-lactalbumin. Propranolol, a beta-adrenergic receptor antagonist, blocked proliferation in all cases except EGF treatment. EGF-induced proliferation could, however, be prevented if the animals were treated with monoclonal antibody to EGF receptor or with the galactosyltransferase modifier alpha-lactalbumin. As a comparison, human parotid tissue samples obtained from neoplastic pleomorphic adenomas, muco-epidermoid carcinoma, adenoid cystic carcinoma, and a bulimia patient were analyzed for galactosyltransferase expression by Northern blot of mRNA and plasma membrane isolation. Elevated levels of galactosyltransferase were found in all neoplastic tissue preparations as well as in the bulimia sample. Amylase synthesis was reduced in samples compared with surrounding normal tissue from the same patient. In vitro cell culturing of pleomorphic adenoma cells in the presence of galactosyltransferase modifier alpha-lactalbumin and substrate UDP-galactose inhibited proliferation in a dose-dependent fashion. Southern blot analysis of DNA from neoplastic parotid cells showed an alteration in chromosomal gene structure for the galactosyltransferase activator cDNA from the adenoid cystic carcinoma. These results for induced acinar cell proliferation as well as human neoplastic pathologies suggest a direct role for cell surface beta 1-4 galactosyltransferase in signaling growth. Furthermore, the proliferation-associated activity of galactosyltransferase suggests that it may be considered as a new type of cell growth regulator.

UR - http://www.scopus.com/inward/record.url?scp=0025440066&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025440066&partnerID=8YFLogxK

M3 - Article

C2 - 2119592

AN - SCOPUS:0025440066

VL - 4

SP - 45

EP - 60

JO - Advances in dental research

JF - Advances in dental research

SN - 0895-9374

ER -