Abstract |
We investigated the effects of the retinoids, all-trans retinoic acid (t-RA), 13-cis retinoic acid, etretinate, and arotinoid ethyl ester, on 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced DNA synthesis, and epidermal hyperplasia in hairless mouse skin. Topical application of these retinoids produced dose-dependent inhibition of the TPA-induced epidermal DNA synthesis as measured by [3H] thymidine incorporation at 15 h after TPA application. However, this inhibition was only transient and did not affect the corresponding increase in epidermal cell layers measured at 40 or 70 h after TPA application. Fluocinonide also inhibited the epidermal DNA synthesis and failed to block TPA-induced epidermal hyperplasia. However, fluocinonide did effectively suppress the inflammation caused by TPA. In this paper we have shown that the suppression of TPA-stimulated DNA synthesis is a general property of topically applied retinoids. The biologic significance of a temporary suppression of TPA-stimulated epidermal DNA synthesis by the retinoids and fluocinonide is not understood at this time.
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Authors | G J Gendimenico, X Nair, P L Bouquin, K M Tramposch |
Journal | The Journal of investigative dermatology
(J Invest Dermatol)
Vol. 93
Issue 3
Pg. 363-7
(Sep 1989)
ISSN: 0022-202X [Print] United States |
PMID | 2768837
(Publication Type: Journal Article)
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Chemical References |
- Retinoids
- Fluocinonide
- DNA
- Tetradecanoylphorbol Acetate
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Topics |
- Animals
- DNA
(biosynthesis)
- Dose-Response Relationship, Drug
- Epidermis
(drug effects, metabolism, pathology)
- Female
- Fluocinonide
(pharmacology)
- Hyperplasia
- Mice
- Mice, Hairless
- Retinoids
(pharmacology)
- Stimulation, Chemical
- Tetradecanoylphorbol Acetate
(pharmacology)
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