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

A Samali, CI Holmberg, Lea Sistonen, S Orrenius

    Tutkimustuotos: LehtiartikkeliArtikkeliTieteellinenvertaisarvioitu

    99 Sitaatiot (Scopus)

    Abstrakti

    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.
    AlkuperäiskieliEi tiedossa
    Sivut306–310
    Sivumäärä5
    JulkaisuFEBS Letters
    Vuosikerta461
    Numero3
    DOI - pysyväislinkit
    TilaJulkaistu - 1999
    OKM-julkaisutyyppiA1 Julkaistu artikkeli, soviteltu

    Keywords

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

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