Pannexin-1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation.

Details

Serval ID
serval:BIB_27CA2505F865
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Pannexin-1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation.
Journal
European journal of immunology
Author(s)
Chen K.W., Demarco B., Broz P.
ISSN
1521-4141 (Electronic)
ISSN-L
0014-2980
Publication state
Published
Issued date
02/2020
Peer-reviewed
Oui
Volume
50
Number
2
Pages
170-177
Language
english
Notes
Publication types: Journal Article
Publication Status: ppublish
Abstract
Inflammasomes are multimeric protein complex that assemble in the cytosol upon microbial infection or cellular stress. Upon activation, inflammasomes drive the maturation of proinflammatory cytokines, IL-1β and IL-18, and also activate the pore-forming protein, gasdermin D to initiate a form of lytic cell death known as "pyroptosis". Pannexin-1 is channel-forming glycoprotein that promotes membrane permeability and ATP release during apoptosis; and was implicated in canonical NLRP3 or noncanonical inflammasome activation. Here, by utilizing three different pannexin-1 channel inhibitors and two lines of Panx1 <sup>-/-</sup> macrophages, we provide genetic and pharmacological evidence that pannexin-1 is dispensable for canonical or noncanonical inflammasome activation. In contrast, we demonstrate that pannexin-1 cleavage and resulting channel activity during apoptosis promotes NLRP3 inflammasome activation.
Keywords
Immunology, Immunology and Allergy, NLRP3, Pannexin-1, apoptosis, caspase-11, gasdermin, inflammasomes, Apoptosis, Caspase-11, Gasdermin, Inflammasomes
Pubmed
Web of science
Create date
15/08/2019 15:08
Last modification date
18/02/2020 7:20
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