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Resources » Paper

Kourtis, Nikos et al. (2010) C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany "Small heat shock proteins protect against necrotic cell death"

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00036898

    Kourtis, Nikos, & Tavernarakis, Nektarios (2010). Small heat shock proteins protect against necrotic cell death presented in C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany. Unpublished information; cite only with author permission.

    Necrotic cell death contributes to severe pathological conditions in humans such as trauma, stroke and neurodegenerative diseases. The molecular mechanisms underlying necrosis are not fully understood. The heat shock response is a highly conserved gene expression program, which is engaged under conditions of stress and orchestrates the coordinated expression of specific genes that protect cells against various stressors. We are investigating the role of the heat shock response in necrotic cell death. We find that activation of the heat shock response pathway by means of a brief heat shock treatment strongly suppresses necrotic cell death caused by harsh environmental conditions, toxic channels, or hypoxia, in C. elegans. This protective effect is not due to delay of necrosis initiation or removal of the necrosis initiating insult. Elimination of heat sho ck factor 1 (HSF-1), the master transcription regulator which orchestrates the heat shock response in C. elegans, abolishes the protective effect of heat shock. By contrast, overexpression of HSF-1 suppresses necrosis. While screening for potential mediators of the protective effect of heat shock, we found that the genes encoding for the small heat shock proteins HSP-16.1 and HSP-16.48 are specifically required for the protective effect of heat shock on necrosis. Moreover, overexpression of HSP-16.1 and HSP-16.48 provides protection against necrotic cell death and circumvents the requirement for heat shock response activation. Further characterization of the protective action of the small heat shock proteins revealed that those proteins modulate calcium release from the Golgi apparatus. Elucidation of the protective mechanism of the heat shock response and HSP-16.1 in necrosis may facilitate the development of intervention strategies aiming to counter necrotic cell death.


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