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Neutrophil extracellular trap cell death requires both autophagy and superoxide generation

Quinten Remijsen UGent, Tom Vanden Berghe UGent, Ellen Wirawan UGent, Bob Asselbergh UGent, Eef Parthoens UGent, Riet De Rycke UGent, Samuel Noppen UGent, Michel Delforge, Jean Willems and Peter Vandenabeele UGent (2011) CELL RESEARCH. 21(2). p.290-304
abstract
Neutrophil extracellular traps (NETs) are extracellular chromatin structures that can trap and degrade microbes. They arise from neutrophils that have activated a cell death program called NET cell death, or NETosis. Activation of NETosis has been shown to involve NADPH oxidase activity, disintegration of the nuclear envelope and most granule membranes, decondensation of nuclear chromatin and formation of NETs. We report that in phorbol myristate acetate (PMA)-stimulated neutrophils, intracellular chromatin decondensation and NET formation follow autophagy and superoxide production, both of which are required to mediate PMA-induced NETosis and occur independently of each other. Neutrophils from patients with chronic granulomatous disease, which lack NADPH oxidase activity, still exhibit PMA-induced autophagy. Conversely, PMA-induced NADPH oxidase activity is not affected by pharmacological inhibition of autophagy. Interestingly, inhibition of either autophagy or NADPH oxidase prevents intracellular chromatin decondensation, which is essential for NETosis and NET formation, and results in cell death characterized by hallmarks of apoptosis. These results indicate that apoptosis might function as a backup program for NETosis when autophagy or NADPH oxidase activity is prevented.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
superoxide, chronic granulomatous disease, granulocyte, neutrophil extracellular trap, autophagy, live cell imaging, NADPH OXIDASE, NET FORMATION, APOPTOSIS, MACROAUTOPHAGY, STREPTOCOCCUS, INVOLVEMENT, INHIBITION, ACTIVATION, MECHANISMS, MATURATION
journal title
CELL RESEARCH
Cell Res.
volume
21
issue
2
pages
290 - 304
Web of Science type
Article
Web of Science id
000286922200008
JCR category
CELL BIOLOGY
JCR impact factor
8.19 (2011)
JCR rank
23/178 (2011)
JCR quartile
1 (2011)
ISSN
1001-0602
DOI
10.1038/cr.2010.150
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1187330
handle
http://hdl.handle.net/1854/LU-1187330
date created
2011-03-14 12:27:15
date last changed
2013-02-27 09:08:15
@article{1187330,
  abstract     = {Neutrophil extracellular traps (NETs) are extracellular chromatin structures that can trap and degrade microbes. They arise from neutrophils that have activated a cell death program called NET cell death, or NETosis. Activation of NETosis has been shown to involve NADPH oxidase activity, disintegration of the nuclear envelope and most granule membranes, decondensation of nuclear chromatin and formation of NETs. We report that in phorbol myristate acetate (PMA)-stimulated neutrophils, intracellular chromatin decondensation and NET formation follow autophagy and superoxide production, both of which are required to mediate PMA-induced NETosis and occur independently of each other. Neutrophils from patients with chronic granulomatous disease, which lack NADPH oxidase activity, still exhibit PMA-induced autophagy. Conversely, PMA-induced NADPH oxidase activity is not affected by pharmacological inhibition of autophagy. Interestingly, inhibition of either autophagy or NADPH oxidase prevents intracellular chromatin decondensation, which is essential for NETosis and NET formation, and results in cell death characterized by hallmarks of apoptosis. These results indicate that apoptosis might function as a backup program for NETosis when autophagy or NADPH oxidase activity is prevented.},
  author       = {Remijsen, Quinten and Vanden Berghe, Tom and Wirawan, Ellen and Asselbergh, Bob and Parthoens, Eef and De Rycke, Riet and Noppen, Samuel and Delforge, Michel and Willems, Jean and Vandenabeele, Peter},
  issn         = {1001-0602},
  journal      = {CELL RESEARCH},
  keyword      = {superoxide,chronic granulomatous disease,granulocyte,neutrophil extracellular trap,autophagy,live cell imaging,NADPH OXIDASE,NET FORMATION,APOPTOSIS,MACROAUTOPHAGY,STREPTOCOCCUS,INVOLVEMENT,INHIBITION,ACTIVATION,MECHANISMS,MATURATION},
  language     = {eng},
  number       = {2},
  pages        = {290--304},
  title        = {Neutrophil extracellular trap cell death requires both autophagy and superoxide generation},
  url          = {http://dx.doi.org/10.1038/cr.2010.150},
  volume       = {21},
  year         = {2011},
}

Chicago
Remijsen, Quinten, Tom Vanden Berghe, Ellen Wirawan, Bob Asselbergh, Eef Parthoens, Riet De Rycke, Samuel Noppen, Michel Delforge, Jean Willems, and Peter Vandenabeele. 2011. “Neutrophil Extracellular Trap Cell Death Requires Both Autophagy and Superoxide Generation.” Cell Research 21 (2): 290–304.
APA
Remijsen, Q., Vanden Berghe, T., Wirawan, E., Asselbergh, B., Parthoens, E., De Rycke, R., Noppen, S., et al. (2011). Neutrophil extracellular trap cell death requires both autophagy and superoxide generation. CELL RESEARCH, 21(2), 290–304.
Vancouver
1.
Remijsen Q, Vanden Berghe T, Wirawan E, Asselbergh B, Parthoens E, De Rycke R, et al. Neutrophil extracellular trap cell death requires both autophagy and superoxide generation. CELL RESEARCH. 2011;21(2):290–304.
MLA
Remijsen, Quinten, Tom Vanden Berghe, Ellen Wirawan, et al. “Neutrophil Extracellular Trap Cell Death Requires Both Autophagy and Superoxide Generation.” CELL RESEARCH 21.2 (2011): 290–304. Print.