Fachbereich Veterinärmedizin


Service-Navigation

    Publikationsdatenbank

    TorsinA protects against oxidative stress in COS-1 and PC12 cells (2003)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Kuner, Rohini
    Teismann, Peter
    Trutzel, Annette
    Naim, Jomana
    Richter, Angelika
    Schmidt, Nicole
    von Ahsen, Oliver
    Bach, Alfred
    Ferger, Boris
    Schneider, Armin
    Quelle
    Neuroscience Letters; 350(3) — S. 153–156
    ISSN: 0304-3940
    Sprache
    Englisch
    Verweise
    Pubmed: 14550917
    Kontakt
    Institut für Pharmakologie und Toxikologie

    Koserstr. 20
    14195 Berlin
    +49 30 838 53221
    pharmakologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Dystonia is a highly frequent movement disorder, the pathogenesis of which remains unclear. The cloning of TorsinA, the gene responsible for early-onset dystonia, was a major breakthrough. However, the function of this protein remains unclear. By sequence homology, TorsinA belongs to the ATPases associated with diverse cellular activities-family, many of whose members are chaperones and/or proteases. We report here that in an in vitro model for oxidative stress, H2O2 treatment, overexpression of TorsinA was protective against cell death. COS-1 cells overexpressing TorsinA demonstrated drastically reduced terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling-staining following exposure to H2O2. Furthermore, transfection with TorsinA significantly increased survival of PC12 after H2O2 treatment. To our knowledge, this is the first demonstration that TorsinA protects against oxidative stress. We speculate that a loss of this cellular function in mutant TorsinA may be linked to the pathogenesis of early-onset dystonia.