Differential sensitivity of inflammatory macrophages and alternatively activated macrophages to ferroptosis.

ABSTRACT: Acumulation of oxidized membrane lipids ultimately results in ferroptotic cell death, which can be prevented by the selenoenzyme glutathione peroxidase 4 (Gpx4). In vivo conditions promoting ferroptosis and susceptible cell types are still poorly defined. In this study, we analyzed the conditional deletion of Gpx4 in mice specifically in the myeloid cell lineages. Surprisingly, development and maintenance of LysM⁺ macrophages and neutrophils, as well as CD11c⁺ monocyte-derived macrophages and dendritic cells were unaffected in the absence of Gpx4. Gpx4-deficient macrophages mounted an unaltered proinflammatory cytokine response including IL-1β production following stimulation with TLR ligands and activation of several inflammasomes. Accordingly, Gpx4^fl/fl L

SUBMITTER: Piattini F 

PROVIDER: S-EPMC9290640 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature