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Effects of Sialagogues on Ornithine Decarboxylase Induction and Proto-oncogene Expression in Murine Parotid Gland

Department of Biochemistry, School of Dentistry, The University of Tokushima, Kuramotocho, Tokushima 770, Japan

A. Ueno

Department of Biochemistry, School of Dentistry, The University of Tokushima, Kuramotocho, Tokushima 770, Japan

Y. Ashida

Department of Biochemistry, School of Dentistry, The University of Tokushima, Kuramotocho, Tokushima 770, Japan

N. Matsumoto

Department of Removable Prosthodontics, School of Dentistry, The University of Tokushima, Kuramotocho, Tokushima 770, Japan

H. Inoue

The mechanism of a sialagogue-induced increase in ornithine decarboxylase (ODC) activity and the expressions of proto-oncogenes in murine parotid gland were investigated by use of isoproterenol (IPR), carbachol (CC), and methoxamine (MTX). The results were as follows: (1) The three sialagogues had similar effects on the parotid in vivo (mouse parotid after a single injection of IPR) and/or in vitro (rat parotid explants cultured on siliconized lens paper floating on 199 medium containing IPR, CC, or MTX), the order of their effectiveness being IPR > CC > MTX. (2) Northern/dot and Western blot analyses revealed that the sialagogues elevated the steady-state levels of ODC mRNA and ODC protein to maxima at two h and six h, respectively, after stimulation. The increases were roughly proportional to those in ODC activity, suggesting that sialagogue-dependent enzyme induction is regulated at the transcriptional level. (3) The mRNAs of four of nine proto-oncogenes examined showed sialagogue-dependent increases to maxima at 30 min (c-fos) or 60 min (c-jun, c-myc, and c-src) after the beginning of stimulation. These increases were all transient, with the levels returning to the control values (without sialagogue) within 60 min. (4) The IPR-dependent elevations of ODC activity and the mRNAs of ODC, c-fos, and c-jun were inhibited by monensin, but not by polymyxin B. On the other hand, the CC-dependent increases in these parameters were inhibited by polymyxin B but not by monensin. The IPR- and CC-induced increases in c-myc and c-src mRNAs were not inhibited by either monensin or polymyxin B, suggesting that the c-Fos and c-Jun proteins participate in this transcriptional control through the AP-1 site of the ODC gene.

Journal of Dental Research, Vol. 71, No. 12, 1885-1890 (1992)
DOI: 10.1177/00220345920710120601


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