Thermotolerance and cell death are distinct cellular responses to stress: dependence on heat shock proteins

A Samali, CI Holmberg, Lea Sistonen, S Orrenius

    Forskningsoutput: TidskriftsbidragArtikelVetenskapligPeer review

    99 Citeringar (Scopus)

    Sammanfattning

    We tested the hypothesis that heat shock protein (Hsp) induction and cell death are mutually exclusive responses to stress. Despite activation of heat shock transcription factor 1 at temperatures ranging from 40 to 46 degrees C, Hsp72 and Hsp27 were not induced above 42 degrees C. Moreover, cells underwent apoptosis at 44 degrees C and necrosis at 46 degrees C, with mitochondrial cytochrome c release at both temperatures. However, only apoptosis was associated with caspase activation. Treatment of cells,vith z-VAD-fmk prior to heat shock at 44 degrees C failed to restore Hsp induction despite inhibition of heat-induced apoptosis. Furthermore, accumulation of Hsps after incubation at 42 degrees C rendered the cells resistant to apoptosis, These results suggest that lack of Hsp induction is the cause rather than the consequence of cell death.
    OriginalspråkOdefinierat/okänt
    Sidor (från-till)306–310
    Antal sidor5
    TidskriftFEBS Letters
    Volym461
    Utgåva3
    DOI
    StatusPublicerad - 1999
    MoE-publikationstypA1 Tidskriftsartikel-refererad

    Nyckelord

    • apoptosis
    • caspase
    • heat shock factor 1
    • heat shock protein
    • necrosis
    • thermotolerance

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