DOI . ORG {}

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We began analyzing https://www.nature.com/articles/cdd200996, but it redirected us to https://www.nature.com/articles/cdd200996. The analysis below is for the second page.

Title[redir]:
Viable neutrophils release mitochondrial DNA to form neutrophil extracellular traps | Cell Death & Differentiation
Description:
Neutrophil extracellular traps (NETs) represent extracellular structures able to bind and kill microorganisms. It is believed that they are generated by neutrophils undergoing cell death, allowing these dying or dead cells to kill microbes. We show that, following priming with granulocyte/macrophage colony-stimulating factor (GM-CSF) and subsequent short-term toll-like receptor 4 (TLR4) or complement factor 5a (C5a) receptor stimulation, viable neutrophils are able to generate NETs. Strikingly, NETs formed by living cells contain mitochondrial, but no nuclear, DNA. Pharmacological or genetic approaches to block reactive oxygen species (ROS) production suggested that NET formation is ROS dependent. Moreover, neutrophil populations stimulated with GM-CSF and C5a showed increased survival compared with resting neutrophils, which did not generate NETs. In conclusion, mitochondrial DNA release by neutrophils and NET formation do not require neutrophil death and do also not limit the lifespan of these cells.

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Keywords {🔍}

dna, neutrophils, mitochondrial, extracellular, cell, death, neutrophil, article, release, figure, stimulation, gmcsf, cells, apoptosis, google, scholar, nature, cas, nuclear, stimulated, nets, formation, traps, blood, net, min, conditions, supplementary, switzerland, structures, released, red, data, viable, yousefi, ros, experiments, gmcsfca, panel, purchased, analysis, information, eosinophils, generation, lps, confocal, microscopy, stained, syto, sytox,

Topics {✒️}

nature portfolio permissions reprints privacy policy granulocyte/macrophage colony-stimulating factor granulocyte-macrophage colony-stimulating factor nature advertising social media author information authors combined gm-csf/lps stimulation combined gm-csf/c5a stimulation development gm-csf/lps stimulation resulted gm-csf/lps stimulated neutrophils gm-csf/lps activated neutrophils agonistic anti-cd95 antibody gm-csf/c5a stimulated neutrophils author correspondence anti-cd95 mab resulted ros-deficient neutrophils derived neutrophil extracellular traps cell death-independent processes combined gm-csf/c5a gm-csf/lps stimulations anti-rabbit secondary abs middle panel phagocytosis-independent antimicrobial activity fitc-conjugated secondary abs c5a-stimulated neutrophils showed 25 ng/ml gm-csf subsequent short-term stimulation live-cell microscopy experiments subsequent short-term toll permissions gm-csf/c5a stimulation short-term cultured neutrophils auto-catabolic activity neutrophil populations stimulated extracellular trap formation fluorescent mounting medium selective fluorescent imaging reactive oxygen species live-cell imaging neutrophil apoptosis pathways initiating neutrophil apoptosis neutrophil apoptosis mediated mbl international corporation privacy permeable sytox orange extracellular mitochondrial dna

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NETosis and kidney disease: what do we know?

Schema {🗺️}

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         description:Neutrophil extracellular traps (NETs) represent extracellular structures able to bind and kill microorganisms. It is believed that they are generated by neutrophils undergoing cell death, allowing these dying or dead cells to kill microbes. We show that, following priming with granulocyte/macrophage colony-stimulating factor (GM-CSF) and subsequent short-term toll-like receptor 4 (TLR4) or complement factor 5a (C5a) receptor stimulation, viable neutrophils are able to generate NETs. Strikingly, NETs formed by living cells contain mitochondrial, but no nuclear, DNA. Pharmacological or genetic approaches to block reactive oxygen species (ROS) production suggested that NET formation is ROS dependent. Moreover, neutrophil populations stimulated with GM-CSF and C5a showed increased survival compared with resting neutrophils, which did not generate NETs. In conclusion, mitochondrial DNA release by neutrophils and NET formation do not require neutrophil death and do also not limit the lifespan of these cells.
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