The acute response of skin cells to oxidative stress and sun irradiation

To timely celebrate one of the hottest and sunniest Summers, the Zamboni lab published a study elucidating a mechanism that allows skin cells to immediately fight oxidative damage before long-term countermeasures are available. We congratulate Andreas, Hila, and our collaborators at Beiersdorf AG

by Nicola Zamboni

 

Abstract

Integrity of human skin is endangered by exposure to UV irradiation and chemical stressors, which can provoke a toxic production of reactive oxygen species (ROS) and oxidative damage. Since oxidation of proteins and metabolites occurs virtually instantaneously, immediate cellular countermeasures are pivotal to mitigate the negative implications of acute oxidative stress. We investigated the short-term metabolic response in human skin fibroblasts and keratinocytes to H2O2 and UV-exposure. In time-resolved metabolomics experiments, we observed that within seconds after stress induction, glucose catabolism is routed to the oxidative pentose phosphate pathway (PPP) and nucleotide synthesis independent of previously postulated blocks in glycolysis, i.e. of GAPDH or PKM2. Through ultra-short 13C labeling experiments, we provide evidence for multiple cycling of carbon backbones in the oxidative PPP, potentially maximizing NADPH reduction. The identified metabolic rerouting in oxidative and non-oxidative PPP has important physiological roles in stabilization of the redox balance and ROS clearance.

 

Reference

Andreas Kuehne, Hila Emmert, Joern Soehle, Marc Winnefeld, Frank Fischer, Horst Wenck, Stefan Gallinat, Lara Terstegen, Ralph Lucius, Janosch Hildebrand, and Nicola Zamboni, Acute activation of oxidative pentose phosphate pathway as first-line response to oxidative  stress in human skin cells, Mol Cell, in press 

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