Plasma membrane perforation by GSDME during ...
Document type :
Article dans une revue scientifique
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Title :
Plasma membrane perforation by GSDME during apoptosis-driven secondary necrosis
Author(s) :
de Schutter, Elke [Auteur]
Universiteit Gent = Ghent University [UGENT]
Ramon, Jana [Auteur]
Universiteit Gent = Ghent University [UGENT]
Pfeuty, Benjamin [Auteur]
Laboratoire de Physique des Lasers, Atomes et Molécules - UMR 8523 [PhLAM]
de Tender, Caroline [Auteur]
Universiteit Gent = Ghent University [UGENT]
Vakgroep Toegepaste Wiskunde en Informatica [Gent] [Department of Applied Mathematics, Computer Science and Statistics]
Stremersch, Stephan [Auteur]
Universiteit Gent = Ghent University [UGENT]
Raemdonck, Koen [Auteur]
Universiteit Gent = Ghent University [UGENT]
de Beeck, Ken Op [Auteur]
Universiteit Gent = Ghent University [UGENT]
Declercq, Wim [Auteur]
Universiteit Gent = Ghent University [UGENT]
Riquet, Franck [Auteur]
Universiteit Gent = Ghent University [UGENT]
Braeckmans, Kevin [Auteur]
Universiteit Gent = Ghent University [UGENT]
Vandenabeele, Peter [Auteur]
Universiteit Gent = Ghent University [UGENT]
Universiteit Gent = Ghent University [UGENT]
Ramon, Jana [Auteur]
Universiteit Gent = Ghent University [UGENT]
Pfeuty, Benjamin [Auteur]
Laboratoire de Physique des Lasers, Atomes et Molécules - UMR 8523 [PhLAM]
de Tender, Caroline [Auteur]
Universiteit Gent = Ghent University [UGENT]
Vakgroep Toegepaste Wiskunde en Informatica [Gent] [Department of Applied Mathematics, Computer Science and Statistics]
Stremersch, Stephan [Auteur]
Universiteit Gent = Ghent University [UGENT]
Raemdonck, Koen [Auteur]
Universiteit Gent = Ghent University [UGENT]
de Beeck, Ken Op [Auteur]
Universiteit Gent = Ghent University [UGENT]
Declercq, Wim [Auteur]
Universiteit Gent = Ghent University [UGENT]
Riquet, Franck [Auteur]

Universiteit Gent = Ghent University [UGENT]
Braeckmans, Kevin [Auteur]
Universiteit Gent = Ghent University [UGENT]
Vandenabeele, Peter [Auteur]
Universiteit Gent = Ghent University [UGENT]
Journal title :
CELLULAR AND MOLECULAR LIFE SCIENCES
Pages :
19
Publisher :
Springer Verlag
Publication date :
2022-01
ISSN :
1420-682X
English keyword(s) :
Gasdermins
Cell death
Membrane permeabilization
Influx
Efflux
Dextrans
Cell death
Membrane permeabilization
Influx
Efflux
Dextrans
HAL domain(s) :
Sciences du Vivant [q-bio]/Biologie cellulaire/Organisation et fonctions cellulaires [q-bio.SC]
English abstract : [en]
Secondary necrosis has long been perceived as an uncontrolled process resulting in total lysis of the apoptotic cell. Recently, it was shown that progression of apoptosis to secondary necrosis is regulated by Gasdermin E ...
Show more >Secondary necrosis has long been perceived as an uncontrolled process resulting in total lysis of the apoptotic cell. Recently, it was shown that progression of apoptosis to secondary necrosis is regulated by Gasdermin E (GSDME), which requires activation by caspase-3. Although the contribution of GSDME in this context has been attributed to its pore-forming capacity, little is known about the kinetics and size characteristics of this. Here we report on the membrane permeabilizing features of GSDME by monitoring the influx and efflux of dextrans of different sizes into/from anti-Fas-treated L929sAhFas cells undergoing apoptosis-driven secondary necrosis. We found that GSDME accelerates cell lysis measured by SYTOX Blue staining but does not affect the exposure of phosphatidylserine on the plasma membrane. Furthermore, loss of GSDME expression clearly hampered the influx of fluorescently labeled dextrans while the efflux happened independently of the presence or absence of GSDME expression. Importantly, both in- and efflux of dextrans were dependent on their molecular weight. Altogether, our results demonstrate that GSDME regulates the passage of compounds together with other plasma membrane destabilizing subroutines.Show less >
Show more >Secondary necrosis has long been perceived as an uncontrolled process resulting in total lysis of the apoptotic cell. Recently, it was shown that progression of apoptosis to secondary necrosis is regulated by Gasdermin E (GSDME), which requires activation by caspase-3. Although the contribution of GSDME in this context has been attributed to its pore-forming capacity, little is known about the kinetics and size characteristics of this. Here we report on the membrane permeabilizing features of GSDME by monitoring the influx and efflux of dextrans of different sizes into/from anti-Fas-treated L929sAhFas cells undergoing apoptosis-driven secondary necrosis. We found that GSDME accelerates cell lysis measured by SYTOX Blue staining but does not affect the exposure of phosphatidylserine on the plasma membrane. Furthermore, loss of GSDME expression clearly hampered the influx of fluorescently labeled dextrans while the efflux happened independently of the presence or absence of GSDME expression. Importantly, both in- and efflux of dextrans were dependent on their molecular weight. Altogether, our results demonstrate that GSDME regulates the passage of compounds together with other plasma membrane destabilizing subroutines.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
Source :
Submission date :
2023-05-07T20:30:45Z
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