Relationship between ornithine decarboxylase activity, ribosomal RNA synthesis and cell proliferation in the mouse uterine epithelium

1985 ◽  
Vol 13 (2) ◽  
pp. 350-351 ◽  
Author(s):  
SHIRLEY V. Y. CHENG ◽  
BARBARA S. MACDONALD ◽  
SAHIRA LARY ◽  
JEFFREY W. POLLARD
Keyword(s):  
Cell Proliferation ◽  
Ornithine Decarboxylase ◽  
Ribosomal Rna ◽  
Rna Synthesis ◽  
Uterine Epithelium ◽  
Decarboxylase Activity ◽  
Ornithine Decarboxylase Activity

scholarly journals Dissociation of tumour-promoter-induced effects on prostaglandin release, polyamine synthesis and cell proliferation of 3T3 cells

1981 ◽  
Vol 194 (3) ◽  
pp. 975-982 ◽  
Author(s):  
R Lanz ◽  
K Brune
Keyword(s):  
Cell Proliferation ◽  
Ornithine Decarboxylase ◽  
Thymidine Incorporation ◽  
Decarboxylase Activity ◽  
3T3 Cells ◽  
Polyamine Synthesis ◽  
Ornithine Decarboxylase Activity ◽  
Proliferative Effect ◽  
Prostaglandin Release ◽  
Anti Inflammatory

The phorbol ester 12-O-tetradecanoylphorbol 13-acetate induces tumour promotion, inflammation, cell proliferation and prostaglandin release. Recent reports suggest that the prostaglandins released by 12-O-tetradecanoylphorbol 13-acetate (TPA) initiate a cascade of events leading to polyamine synthesis and cell proliferation. In experiments designed to test this contention, it was found that addition of TPA (1 microM to 1 nM) to confluent mouse 3T3 fibroblasts successively caused the release of prostaglandins E2 and I2, induction of the enzyme ornithine decarboxylase (EC 4.1.1.17), stimulation of [3H]thymidine incorporation into DNA, and cell proliferation. Pretreatment of the cells with the anti-inflammatory steroid dexamethasone (1 microM) or the non-steroidal anti-inflammatory drug indomethacin (1 microM) inhibited TPA-induced prostaglandin release. However, dexamethasone enhanced the other effects of TPA, whereas indomethacin was ineffective. Addition of prostaglandin E2 to the cultures did not induce ornithine decarboxylase activity and cell proliferation. Pretreatment of the cells with 1,3-diaminopropane (1 mM) or alpha-methylornithine (5 mM), inhibitors of polyamine synthesis, decreased TPA-induced ornithine decarboxylase activity without affecting DNA synthesis. TPA stimulated [3H]thymidine incorporation into DNA, even when the ornithine decarboxylase activity was completely blocked. These data suggest that the proliferative effect of TPA on 3T3 cells is independent of prostaglandin release and polyamine synthesis.

Effects of 4-Hydroxynonenal, A Product of Lipid Peroxidation, on Cell Proliferation and Ornithine Decarboxylase Activity

1991 ◽  
Vol 14 (2) ◽  
pp. 81-89 ◽  
Author(s):  
Giuseppina Barrera ◽  
Olga Brossa ◽  
Vito Michele Fazio ◽  
Maria Giulia Farace ◽  
Luciana Paradisi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cell Proliferation ◽  
Ornithine Decarboxylase ◽  
Decarboxylase Activity ◽  
Ornithine Decarboxylase Activity

scholarly journals Control of ornithine decarboxylase activity in stimulated human lymphocytes by putrescine and spermidine

1973 ◽  
Vol 132 (4) ◽  
pp. 791-796 ◽  
Author(s):  
John E. Kay ◽  
Valerie J. Lindsay
Keyword(s):  
Protein Synthesis ◽  
Ornithine Decarboxylase ◽  
Rna Synthesis ◽  
Culture Medium ◽  
Feedback Inhibition ◽  
Human Lymphocytes ◽  
Decarboxylase Activity ◽  
Ornithine Decarboxylase Activity

Ornithine decarboxylase activity in extracts of phytohaemagglutinin-stimulated human lymphocytes is rapidly and extensively inhibited by additions of micromolar concentrations of putrescine or spermidine to the culture medium. This inhibition is not due to feedback inhibition of the enzyme by putrescine, spermidine or their metabolites. Inhibition is dependent on the continuation of protein synthesis, but does not require RNA synthesis. The effect of putrescine is abolished when its conversion into spermidine by the cells is prevented.

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