Published February 21, 2025 | Version v1

Ferroptosis spreads to neighboring cells via plasma membrane contacts

  • 1. Institute for Genetics, University of Cologne, 50931 Cologne, Germany
  • 2. CECAD Cluster of Excellence, University of Cologne, 50931 Cologne, Germany
  • 3. University of Cologne, Faculty of Medicine and University Hospital of Cologne, Cluster of Excellence Cellular Stress Responses in Aging-associated Diseases (CECAD), 50931 Cologne, Germany
  • 4. Max Planck Institute of Biophysics, Frankfurt, Germany
  • 1. Institute for Genetics, University of Cologne, 50931 Cologne, Germany
  • 2. CECAD Cluster of Excellence, University of Cologne, 50931 Cologne, Germany
  • 3. Max Planck Institute of Biophysics, Frankfurt, Germany
  • 4. Department of Translational Genomics, Center of Integrated Oncology Cologne-Bonn, Medical Faculty, University of Cologne, 50931 Cologne, Germany
  • 5. Center for Molecular Medicine Cologne, Medical Faculty, University Hospital of Cologne, 50931 Cologne, Germany

Description

The uploaded lipidomics dataset contains Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS) data associated to the publication of Bernhard F. Roeck et al. from the laboratory of Ana J. Garcia-Saez. 

The title of the publication is:

Ferroptosis spreads to neighboring cells via plasma membrane contacts

This article is to be published in Nature Communications.

Article Abstract

Ferroptosis is a lytic, iron-dependent form of regulated cell death characterized by excessive lipid peroxidation and associated with necrosis spread in diseased tissues through unknown mechanisms. Using a novel optogenetic system for light-driven ferroptosis induction via degradation of the anti-ferroptotic protein GPX4, we show that lipid peroxidation and ferroptotic death can spread to neighboring cells through their closely adjacent plasma membranes. Ferroptosis propagation was dependent on cell distance and completely abolished by disruption of a-catenin-dependent intercellular contacts or by chelation of extracellular iron. Remarkably, bridging cells with a lipid bilayer or increasing contacts between neighboring cells enhanced ferroptosis spread. Reconstitution of iron-dependent spread of lipid peroxidation between pure lipid, contacting liposomes provides evidence for the physicochemical mechanism involved. Our findings support a model in which iron-dependent lipid peroxidation propagates across proximal plasma membranes of neighboring cells, thereby promoting the transmission of ferroptotic cell death with consequences for pathological tissue necrosis spread.

 

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