Publication: Gasdermin D mediates a fast transient release of ATP after NLRP3 inflammasome activation before ninjurin 1-induced lytic cell death
Authors
Schachter, Julieta ; Guijarro, Adriana ; Angosto-Bazarra, Diego ; Pinilla, Miriam ; Hurtado-Navarro, Laura ; Meunier, Etienne ; Perez-Oliva, Ana Belen ; Schwarzbaum, Pablo J ; Pelegrín Vivancos, Pablo ; Pinilla Marquinez, Míriam
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Publisher
Cell Press
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DOI
https://doi.org/ 10.1016/j.celrep.2025.115233
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info:eu-repo/semantics/article
Description
©2025. This manuscript version is made available under the CC-BY 4.0 license http://creativecommons.org/licenses/by/4.0/
This document is the published version of a Published Work that appeared in final form in Cell Reports. To access the final edited and published work see https://doi.org/ 10.1016/j.celrep.2025.115233
Abstract
Pyroptosis is a lytic cell death triggered by the cleavage of gasdermin (GSDM) proteins and subsequent pore formation by the N-terminal domain oligomerization in the plasma membrane. GSDMD is cleaved by caspase-1/-4/-5/-11 upon inflammasome activation and mediates interleukin (IL)-1β and IL-18 release. GSDMD pores favor ninjurin 1 (NINJ1)-induced plasma membrane rupture and cell death. Here, we demonstrate that GSDMD mediates early ATP release upon NLRP3 inflammasome activation independently of NINJ1, occurring before IL-1β release and cell death and constituting an early danger signal. The release of ATP is a transient signal terminated before the cells continue to permeabilize and die. The different N termini of GSDMA to -E are also able to release ATP and induce monocyte migration toward pyroptotic cells. This study reveals ATP release as an early and transient danger signal depending on GSDMD plasma membrane permeabilization, independently of the late stages of lytic cell death.
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Citation
Cell Reports 44(2)
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