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    Regulation of uncoupling protein-2 (UCP-2) expression in human glioma cells by peroxisome proliferators-activated receptor (PPAR) agonists

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    Authors
    Brown, James E. P.
    Darling, John L.
    Dunmore, Simon J.
    Bassey, S.
    Issue Date
    2005
    
    Metadata
    Show full item record
    Other Titles
    In: Abstracts from the World Federation of Neuro-Oncology 2nd Quadrennial Meeting and the 6th Meeting of the European Association for Neuro-Oncology, May 5–8, 2005, Edinburgh, UK. No.56
    Abstract
    Recent studies have suggested that the glitazones, a group of PPAR agonists commonly prescribed as therapy in type 2 diabetes, could have a role in regulation of cell viability in astrocytomas and glioma cell lines, possibly due to a modulation of reactive oxygen species (ROS) production. PPAR agonists are also known to regulate expression of the mitochondrial protein UCP-2, and UCP-2 has a purported role in ROS regulation amongst others. This study investigated the expression of UCP-2 in U251MG glioma cells and its regulation by PPAR agonists. U251MG glioma cells were cultured according to standard methods and treated with PPAR alpha, delta, and gamma agonists (10 μM WY14643, 10 nM PGI2, 10 μM rosiglitazone and 10 nM PGJ2, respectively) for 24 h. Total RNA was subsequently extracted and semiquantitative RT-PCR used to evaluate UCP-2 mRNA expression. Results showed that UCP-2 was expressed in all control and treatment samples and that its expression was regulated differentially by the various PPAR receptor subtype agonists tested. This novel finding that UCP-2 is expressed in glioma cells, and that its expression is regulated by PPAR agonists, suggests a potential mechanism for the cytotoxic effects of glitazones that have been previously reported, and describes a mechanism which could possibly be manipulated as a potential therapeutic avenue in the future.
    Citation
    Neuro-oncology, 7(3): 296
    Publisher
    Society for Neuro-Oncology and Duke University Press
    Journal
    Neuro-oncology
    URI
    http://hdl.handle.net/2436/29933
    Additional Links
    http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1871910
    Type
    Conference contribution
    Language
    en
    Description
    Abstracts from Neuro-Oncology are provided here courtesy of Society for Neuro-Oncology and Duke University Press
    ISSN
    1522-8517
    Collections
    Research Institute in Healthcare Science

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