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Comparison of inhibition by a tumor promoter (12-O-tetradecanoylphorbol-13-acetate) of expression of the differentiated phenotype of chondrocytes in rabbit costal chondrocytes in culture with inhibition by retinoic acid.
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- Additional Information
- Source:
Publisher: Oxford University Press Country of Publication: England NLM ID: 0376600 Publication Model: Print Cited Medium: Print ISSN: 0021-924X (Print) Linking ISSN: 0021924X NLM ISO Abbreviation: J Biochem Subsets: MEDLINE
- Publication Information:
Publication: : Abingdon, UK : Oxford University Press
Original Publication: Tokyo : Japanese Biochemical Society
- Subject Terms:
- Abstract:
Both retinoids and the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibit expression of the differentiated phenotype by rabbit costal chondrocytes in culture, as judged by morphological changes and decreased sulfation of glycosaminoglycans (GAG). However, the inhibition of the differentiated phenotype of chondrocytes in TPA-treated cells is restored by parathyroid hormone (PTH), while the inhibition by retinoids is not [Takigawa et al. (1982) Mol. Cell. Biochem. 42, 145-153; Takigawa et al. (1983) Cell Differ. 13, 283-291]. In the present study, we examined the difference between TPA-treated chondrocytes and retinoic acid-treated chondrocytes to determine the mechanism of the restoration of the differentiated phenotype in de-differentiated cells treated with TPA. PTH increased the activity of ornithine decarboxylase [ODC; EC 4.1.1.17], a rate limiting enzyme of polyamine biosynthesis, and proteoglycan synthesis in chondrocytes pretreated with TPA as well as in normal chondrocytes. The maximal stimulations of ODC activity and GAG synthesis were observed 4 h and 24-36 h, respectively, after addition of PTH. The dose-response curve for ODC induction by PTH was parallel to that of PTH-stimulated proteoglycan synthesis both in TPA-treated chondrocytes and in normal chondrocytes. PTH also increased the intracellular cyclic AMP level after 2 min in TPA-treated cells as in normal cells. Addition of dibutyryl cyclic AMP (DBcAMP) induced ODC and restored proteoglycan synthesis in TPA-treated cells. The dose-response curve for induction of ODC by DBcAMP was parallel to that of DBcAMP-stimulated proteoglycan synthesis in both TPA-treated chondrocytes and normal chondrocytes. On the other hand, the increases by PTH in the intracellular cyclic AMP level, ODC activity, and proteoglycan synthesis were inhibited in chondrocytes pretreated with a combination of TPA and retinoic acid as well as in those pretreated with retinoic acid alone. TPA stimulated the syntheses of DNA and RNA in chondrocytes but did not increase the cyclic AMP level or ODC activity. PTH and DBcAMP inhibited the syntheses of DNA and RNA both in TPA-treated cells and in normal cells. These results suggest that ODC induction mediated by elevation of cyclic AMP plays an important role in re-differentiation of de-differentiated cells pretreated with these agents.
- Accession Number:
0 (Glycosaminoglycans)
0 (Parathyroid Hormone)
0 (Phorbols)
0 (Proteoglycans)
5688UTC01R (Tretinoin)
63X7MBT2LQ (Bucladesine)
E0399OZS9N (Cyclic AMP)
EC 4.1.1.17 (Ornithine Decarboxylase)
NI40JAQ945 (Tetradecanoylphorbol Acetate)
- Publication Date:
Date Created: 19860201 Date Completed: 19860609 Latest Revision: 20190510
- Publication Date:
20240829
- Accession Number:
10.1093/oxfordjournals.jbchem.a135493
- Accession Number:
3009424
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