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Age-dependent heat shock hormesis to HSF-1 deficiency suggests a compensatory mechanism mediated by the unfolded protein response and innate immunity in young Caenorhabditis elegans.
Kovács, Dániel; Biró, János Barnabás; Ahmed, Saqib; Kovács, Márton; Sigmond, Tímea; Hotzi, Bernadette; Varga, Máté; Vincze, Viktor Vázsony; Mohammad, Umar; Vellai, Tibor; Barna, János.
Afiliación
  • Kovács D; Department of Genetics, ELTE Eötvös Loránd University, Budapest, Hungary.
  • Biró JB; Department of Genetics, ELTE Eötvös Loránd University, Budapest, Hungary.
  • Ahmed S; Department of Genetics, ELTE Eötvös Loránd University, Budapest, Hungary.
  • Kovács M; Department of Genetics, ELTE Eötvös Loránd University, Budapest, Hungary.
  • Sigmond T; Department of Genetics, ELTE Eötvös Loránd University, Budapest, Hungary.
  • Hotzi B; Department of Genetics, ELTE Eötvös Loránd University, Budapest, Hungary.
  • Varga M; Department of Genetics, ELTE Eötvös Loránd University, Budapest, Hungary.
  • Vincze VV; Department of Genetics, ELTE Eötvös Loránd University, Budapest, Hungary.
  • Mohammad U; Department of Genetics, ELTE Eötvös Loránd University, Budapest, Hungary.
  • Vellai T; Department of Genetics, ELTE Eötvös Loránd University, Budapest, Hungary.
  • Barna J; HUN-REN-ELTE Genetics Research Group, Eötvös Loránd University, Budapest, Hungary.
Aging Cell ; : e14246, 2024 Jun 19.
Article en En | MEDLINE | ID: mdl-38895933
ABSTRACT
The transcription factor HSF-1 (heat shock factor 1) acts as a master regulator of heat shock response in eukaryotic cells to maintain cellular proteostasis. The protein has a protective role in preventing cells from undergoing ageing, and neurodegeneration, and also mediates tumorigenesis. Thus, modulating HSF-1 activity in humans has a promising therapeutic potential for treating these pathologies. Loss of HSF-1 function is usually associated with impaired stress tolerance. Contrary to this conventional knowledge, we show here that inactivation of HSF-1 in the nematode Caenorhabditis elegans results in increased thermotolerance at young adult stages, whereas HSF-1 deficiency in animals passing early adult stages indeed leads to decreased thermotolerance, as compared to wild-type. Furthermore, a gene expression analysis supports that in young adults, distinct cellular stress response and immunity-related signaling pathways become induced upon HSF-1 deficiency. We also demonstrate that increased tolerance to proteotoxic stress in HSF-1-depleted young worms requires the activity of the unfolded protein response of the endoplasmic reticulum and the SKN-1/Nrf2-mediated oxidative stress response pathway, as well as an innate immunity-related pathway, suggesting a mutual compensatory interaction between HSF-1 and these conserved stress response systems. A similar compensatory molecular network is likely to also operate in higher animal taxa, raising the possibility of an unexpected outcome when HSF-1 activity is manipulated in humans.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Aging Cell Año: 2024 Tipo del documento: Article País de afiliación: Hungria Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Aging Cell Año: 2024 Tipo del documento: Article País de afiliación: Hungria Pais de publicación: Reino Unido