Document Detail


Regulation of ultraviolet B radiation-mediated activation of AP1 signaling by retinoids in primary keratinocytes.
MedLine Citation:
PMID:  15733037     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The main cause of skin cancer and photo-aging is chronic exposure to ultraviolet B (UVB) radiation. Such damage can be ameliorated by retinoid treatment. UVB-radiation-induced skin carcinogenesis is associated with the induction of activator protein 1 (AP1) signaling and factors, namely FOS and JUN family members. We investigated the effects of several retinoids, all-trans-retinoic acid (tRA), 9-cis-retinoic acid (cRA), and N-(4-hydroxyphenyl)-retinamide (HPR), on UVB-induced damage in primary mouse keratinocytes. In addition, the interplay between UVB radiation, retinoid receptors, and AP1 signaling was assessed using Western blot analysis and ribonuclease protection and gene reporter assays. Exposure of keratinocytes to UVB radiation caused a down-regulation of the retinoid receptor protein levels in a proteasome-mediated manner. In contrast, FOS and JUN proteins were transiently induced shortly after exposure to UVB radiation. Retinoid treatment caused a dose-dependent reduction in the levels of retinoid receptor proteins. When irradiated cells were treated with retinoids, no significant effects on AP1 protein expression were noted. Interestingly, pretreatments with tRA and cRA, but not HPR, suppressed UVB-radiation-induced AP1 activity by more than 50%, whereas post-treatment failed to produce similar effects. Our findings indicate that the inhibition of AP1 activity by retinoids explains, at least in part, the chemopreventive potential of retinoids in UV-radiation-associated epidermal damage.
Authors:
Nadine Darwiche; Hisham Bazzi; Lara El-Touni; Ghada Abou-Lteif; Rami Doueiri; Asma Hatoum; Samar Maalouf; Hala Gali-Muhtasib
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Radiation research     Volume:  163     ISSN:  0033-7587     ISO Abbreviation:  Radiat. Res.     Publication Date:  2005 Mar 
Date Detail:
Created Date:  2005-02-28     Completed Date:  2005-04-07     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0401245     Medline TA:  Radiat Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  296-306     Citation Subset:  IM; S    
Affiliation:
Department of Biology, American University of Beirut, Beirut, Lebanon. darwichn@aub.edu.lb
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MeSH Terms
Descriptor/Qualifier:
Animals
Antineoplastic Agents / pharmacology
Blotting, Western
Cell Line
Dose-Response Relationship, Radiation
Down-Regulation
Epidermis / metabolism
Fenretinide / pharmacology
Gene Expression Regulation
Genes, Reporter
Keratinocytes / cytology*,  metabolism,  radiation effects*
Luciferases / metabolism
Mice
Proteasome Endopeptidase Complex / metabolism
Proto-Oncogene Proteins c-fos / metabolism
Proto-Oncogene Proteins c-jun / metabolism
Retinoids / metabolism
Signal Transduction
Skin Neoplasms / etiology
Time Factors
Transcription Factor AP-1 / metabolism*
Transfection
Tretinoin / metabolism
Ultraviolet Rays*
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/Proto-Oncogene Proteins c-fos; 0/Proto-Oncogene Proteins c-jun; 0/Retinoids; 0/Transcription Factor AP-1; 302-79-4/Tretinoin; 65646-68-6/Fenretinide; EC 1.13.12.-/Luciferases; EC 3.4.25.1/Proteasome Endopeptidase Complex

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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