Nerve growth factor-induced increase in [3H]thymidine incorporation into parotid and submandibular glands of young rats and its partial blockade by propranolol or partial sialoadenectomy

Biochemical Pharmacology
C A Schneyer, M G Humphreys-Beher

Abstract

Administration of nerve growth factor (NGF) twice daily for 2 days to young rats (11 days old at the time of the initial injection) resulted in an 8.1-fold increase in [3H]thymidine levels of the parotid gland, and a 9.7-fold increase in levels of the submandibular gland when compared to untreated controls. Isoproterenol (ISO), a beta-adrenergic receptor agonist, caused an 8.7-fold increase in [3H]thymidine incorporation into DNA of the parotid gland, and a 10.7-fold increase in [3H]thymidine in the submandibular gland when compared to controls. The increase in thymidine was accompanied by parotid gland enlargement as well as an increase in cell surface beta 1-4 galactosyltransferase, an enzyme whose expression has been associated previously with acinar cell proliferation. Administration of NGF and ISO together were not additive in their effects on the parotid and submandibular glands. The introduction of propranolol, a beta-adrenergic receptor antagonist, completely negated the ISO effects on the salivary glands but was only partially effective in blocking the NGF effects on the glands. An assay of parotid levels of norepinephrine showed NGF treatment to cause an increase in gland-associated levels of neurotransmitter. Removal...Continue Reading

References

Mar 1, 1977·Proceedings of the National Academy of Sciences of the United States of America·J T LaMontK J Isselbacher
Feb 1, 1978·Pediatric Research·R J Grand, M I Schay
Jan 1, 1979·Cell and Tissue Research·J H Sheetz, L Menaker
Feb 14, 1978·Cell and Tissue Research·H D Hall, C A Schneyer
Jun 1, 1988·Proceedings of the Society for Experimental Biology and Medicine·C A Schneyer, M Humphreys-Beher
Feb 1, 1988·Proceedings of the National Academy of Sciences of the United States of America·P Masiakowski, E M Shooter
Dec 1, 1986·Proceedings of the National Academy of Sciences of the United States of America·L R WilliamsF H Gage
Sep 1, 1974·Endocrinology·R L ByynyE S Doyne
Feb 1, 1972·Proceedings of the National Academy of Sciences of the United States of America·S Roth, D White
Feb 1, 1973·Analytical Biochemistry·G R Schacterle, R L Pollack
Jul 1, 1968·Physiological Reviews·R Levi-Montalcini, P U Angeletti
Jul 1, 1970·The Journal of Cell Biology·R S Redman, L M Sreebny
Feb 1, 1969·Proceedings of the Society for Experimental Biology and Medicine·C A Schneyer, H D Hall
Sep 1, 1969·Proceedings of the Society for Experimental Biology and Medicine·H D Hall, C A Schneyer
Jan 1, 1980·Annual Review of Neuroscience·L A Greene, E M Shooter
Jan 1, 1984·Molecular and Cellular Biochemistry·B D Shur
Aug 1, 1980·The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society·R A MurphyW G Forssmann
Jan 1, 1980·International Review of Cytology·M PierceS Roth
Nov 1, 1961·The American Journal of Physiology·C A SCHNEYER, L H SCHNEYER
Aug 1, 1962·The American Journal of Physiology·C A SCHNEYER
Feb 1, 1963·Proceedings of the Society for Experimental Biology and Medicine·C A SCHNEYER, J M SHACKLEFORD

❮ Previous
Next ❯

Citations

May 7, 2003·Biochemical Pharmacology·Takashi TakeuchiRonald P Rubin
Oct 13, 2009·Memórias do Instituto Oswaldo Cruz·Kezia L H AguirreAnderson J Ferreira

❮ Previous
Next ❯

Related Concepts

Related Feeds

Adrenergic Receptors: Trafficking

Adrenergic receptor trafficking is an active physiological process where adrenergic receptors are relocated from one region of the cell to another or from one type of cell to another. Discover the latest research on adrenergic receptor trafficking here.