Heat stress downregulates FLIP and sensitizes cells to Fas receptor-mediated apoptosis

Tran SEF, Annika Meinander, TH Holmström, A Rivero-Muller, KM Heiskanen, EK Linnau, MJ Courtney, DD Mosser, Lea Sistonen, John Eriksson

    Tutkimustuotos: LehtiartikkeliArtikkeliTieteellinenvertaisarvioitu

    47 Sitaatiot (Scopus)

    Abstrakti

    The heat shock response and death receptor-mediated apoptosis are both key physiological determinants of cell survival. We found that exposure to a mild heat stress rapidly sensitized Jurkat and HeLa cells to Fas-mediated apoptosis. We further demonstrate that Hsp70 and the mitogen-activated protein kinases, critical molecules involved in both stress-associated and apoptotic responses, are not responsible for the sensitization. Instead, heat stress on its own induced downregulation of FLIP and promoted caspase-8 cleavage without triggering cell death, which might be the cause of the observed sensitization. Since caspase-9 and -3 were not cleaved after heat shock, caspase-8 seemed to be the initial caspase activated in the process. These findings could help understanding the regulation of death receptor signaling during stress, fever, or inflammation.
    AlkuperäiskieliEi tiedossa
    Sivut1137–1147
    Sivumäärä11
    JulkaisuCell Death and Differentiation
    Vuosikerta10
    Numero10
    DOI - pysyväislinkit
    TilaJulkaistu - 2003
    OKM-julkaisutyyppiA1 Julkaistu artikkeli, soviteltu

    Keywords

    • apoptosis
    • caspase
    • CD95
    • death receptor
    • Fas
    • FLIP
    • heat shock
    • stress

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