Journal Article

Expression of PGF<sub>2α</sub> receptor mRNA in normal, hyperplastic and neoplastic skin

Karsten Müller, Peter Krieg, Friedrich Marks and Gerhard Fürstenberger

in Carcinogenesis

Volume 21, issue 5, pages 1063-1066
Published in print May 2000 | ISSN: 0143-3334
Published online May 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.5.1063
Expression of PGF2α receptor mRNA in normal, hyperplastic and neoplastic skin

More Like This

Show all results sharing this subject:

  • Clinical Cytogenetics and Molecular Genetics

GO

Show Summary Details

Preview

Reverse transcription polymerase chain reaction (RT–PCR) and Northern blot analysis was used to determine the level of expression of prostaglandin F (FP) receptor mRNA in various mouse tissues, including normal, hyperplastic and neoplastic mouse epidermis. Steady-state concentrations of FP receptor mRNA were low in normal and hyperplastic epidermis. The response of the epidermis to the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) was biphasic in that FP receptor mRNA was increased immediately after treatment, followed by a long-lasting down-regulation at later time points. FP receptor mRNA was down-regulated in the majority of papillomas obtained by the mouse skin carcinogenesis initiation–promotion protocol. In carcinomas, FP receptor mRNA expression was similar to that in normal epidermis. The steady-state concentration of FP mRNA was inversely correlated with PGF levels in normal and hyperplastic epidermis and in papillomas, indicating that FP mRNA expression is regulated by this eicosanoid.

Keywords: NSAID, non-steroidal anti-inflammatory drug; PGF2α, prostaglandin F2α; FP receptor, PGF2α receptor; TPA, 12-O-tetradecanoylphorbol-13-acetate.

Journal Article.  2728 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.