Ferritin-mediated iron detoxification promotes hypothermia survival in Caenorhabditis elegans and murine neurons

Tina Pekec, Jarosław Lewandowski, Alicja A. Komur, Daria Sobańska, Yanwu Guo, Karolina Świtońska-Kurkowska, Jędrzej M. Małecki, Abhishek Anil Dubey, Wojciech Pokrzywa, Marcin Frankowski, Maciej Figiel and Rafal Ciosk ()
Additional contact information
Tina Pekec: Friedrich Miescher Institute for Biomedical Research
Jarosław Lewandowski: Polish Academy of Sciences
Alicja A. Komur: Polish Academy of Sciences
Daria Sobańska: Polish Academy of Sciences
Yanwu Guo: University of Oslo, Department of Biosciences
Karolina Świtońska-Kurkowska: Polish Academy of Sciences
Jędrzej M. Małecki: University of Oslo, Department of Biosciences
Abhishek Anil Dubey: International Institute of Molecular and Cell Biology in Warsaw
Wojciech Pokrzywa: International Institute of Molecular and Cell Biology in Warsaw
Marcin Frankowski: Adam Mickiewicz University in Poznań, Faculty of Chemistry
Maciej Figiel: Polish Academy of Sciences
Rafal Ciosk: Polish Academy of Sciences

Nature Communications, 2022, vol. 13, issue 1, 1-19

Abstract: Abstract How animals rewire cellular programs to survive cold is a fascinating problem with potential biomedical implications, ranging from emergency medicine to space travel. Studying a hibernation-like response in the free-living nematode Caenorhabditis elegans, we uncovered a regulatory axis that enhances the natural resistance of nematodes to severe cold. This axis involves conserved transcription factors, DAF-16/FoxO and PQM-1, which jointly promote cold survival by upregulating FTN-1, a protein related to mammalian ferritin heavy chain (FTH1). Moreover, we show that inducing expression of FTH1 also promotes cold survival of mammalian neurons, a cell type particularly sensitive to deterioration in hypothermia. Our findings in both animals and cells suggest that FTN-1/FTH1 facilitates cold survival by detoxifying ROS-generating iron species. We finally show that mimicking the effects of FTN-1/FTH1 with drugs protects neurons from cold-induced degeneration, opening a potential avenue to improved treatments of hypothermia.

Date: 2022
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DOI: 10.1038/s41467-022-32500-z

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