Defects in intracellular oxidative metabolism of neutrophils undergoing apoptosis

Narayanan, Padma K.; Ragheb, Kathy; Lawler, Gretchen; Robinson, J. Paul

doi:10.1002/jlb.61.4.481

Cited by 45 publications

(25 citation statements)

References 47 publications

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“…Gustafsson et al 7) showed that PMA induces intracellular H 2 O 2 production and a rapid onset of apoptosis in human neutrophils. Narayanan et al 21) suggested that the onset of apoptosis in PMA-activated neutrophils is partly due to oxidative stress induced by down-regulation of the antioxidants superoxide dismutase and glutathione, which leads to intracellular accumulation of O 2 À , but the target molecule of O 2 À has remained to be identified. In the present study, we showed that PMA-induced cell death of mouse neutrophils was caspase-independent, A, PKC inhibitor GF109203X blocked PMA-induced phosphorylation of p38 MAPK.…”

Section: Discussionmentioning

confidence: 99%

Phorbol Myristate Acetate Induces Neutrophil Death through Activation of p38 Mitogen-Activated Protein Kinase That Requires Endogenous Reactive Oxygen Species Other Than HOCl

Saito

Takahashi

Doken

et al. 2005

Bioscience, Biotechnology, and Biochemistry

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Section: Discussionmentioning

confidence: 99%

Phorbol Myristate Acetate Induces Neutrophil Death through Activation of p38 Mitogen-Activated Protein Kinase That Requires Endogenous Reactive Oxygen Species Other Than HOCl

Saito

Takahashi

Doken

et al. 2005

Bioscience, Biotechnology, and Biochemistry

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“…Narayanan and colleagues [50] suggested that the onset of apoptosis in neutrophils is partly due to oxidative stress induced by down-regulation of the antioxidants superoxide dismutase (SOD) and glutathione, which leads to intracellular accumulation of …”

Section: Discussionmentioning

confidence: 99%

Activation of the granule pool of the NADPH oxidase accelerates apoptosis in human neutrophils

Lundqvist-Gustafsson

Bengtsson

1999

Journal of Leukocyte Biology

135

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Oxidative stress induces apoptosis in many types of cells, including human neutrophils. Our objective was to determine whether reactive oxygen species (ROS) produced by activated neutrophils are associated with accelerated apoptosis. Exposing neutrophils to ionomycin or phorbol myristate acetate (PMA) induced intracellular H 2 O 2 production and rapid onset of apoptosis, measured as condensed chromatin, cellular shrinkage, and DNA fragmentation. Neutrophils activated with formyl-methionyl-leucyl-phenylalanine (fMLP) generated mainly extracellular H 2 O 2 and did not undergo apoptosis. Exogenously added H 2 O 2 , together with the catalase blocker sodium azide, induced apoptosis to the same extent and with similar kinetics as PMA and ionomycin. Adenosine inhibited ionomycin-induced intracellular H 2 O 2 production and apoptosis. Neither PMA nor ionomycin caused apoptosis in dimethyl sulfoxide-differentiated HL-60 cells, which are incapable of intracellular H 2 O 2 production, whereas H 2 O 2 induced apoptosis more efficiently in these cells than in neutrophils. We propose that activated neutrophils use intracellularly formed H 2 O 2 to commit suicide.

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“…Conversely, when neutrophils reach a site of inflammation, apoptosis is delayed by inflammatory cytokines in the tissues, providing additional time for completion of the neutrophil's microbicidal function (8). However, neutrophils also become activated when they migrate from the blood; their subsequent production of ROS generates oxidative stress that instigates apoptosis (9,10). Redox-dependent mechanisms for apoptosis include the intracellular production of superoxide (O 2 . )…”

mentioning

confidence: 99%

“…Redox-dependent mechanisms for apoptosis include the intracellular production of superoxide (O 2 . ) and hydrogen peroxide (H 2 O 2 ) by activation of the NADPH oxidase in the granule pool (9) or the down-regulation of key antioxidant systems of the cell, such as superoxide dismutase (SOD), and a decrease in GSH (10). In addition, macrophages and phagocytic cells in the inflammatory area release Fas ligand during phagocytosis, contributing further to triggering apoptosis in neutrophils (11).…”

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confidence: 99%

NADPH Oxidase-dependent Oxidation and Externalization of Phosphatidylserine during Apoptosis in Me2SO-differentiated HL-60 Cells

Arroyo

Modrianský²,

Serinkan³

et al. 2002

Journal of Biological Chemistry

128

103

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Resolution of inflammation requires clearance of activated neutrophils by phagocytes in a manner that protects adjacent tissues from injury. Mechanisms governing apoptosis and clearance of activated neutrophils from inflamed areas are still poorly understood. We used dimethylsulfoxide-differentiated HL-60 cells showing inducible oxidase activity to study NADPH oxidase-induced apoptosis pathways typical of neutrophils. Activation of the NADPH oxidase by phorbol myristate acetate caused oxidative stress as shown by production of superoxide and hydrogen peroxide, depletion of intracellular glutathione, and peroxidation of all three major classes of membrane phospholipids, phosphatidylcholine, phosphatidylethanolamine, and phosphatidylserine. In addition, phorbol myristate acetate stimulation of the NADPH oxidase caused apoptosis, as evidenced by apoptosis-specific phosphatidylserine externalization, increased caspase-3 activity, chromatin condensation, and nuclear fragmentation. Neutrophils aid host defense by killing invading microorganisms through production of highly reactive oxygen species (ROS) 1 generated by activation of the NADPH oxidase complex. When released inappropriately into the extracellular milieu, these ROS can cause persistent inflammation and considerable damage to the surrounding, healthy tissues. To prevent calamitous release of ROS, macrophages remove excess activated neutrophils from an inflammatory site in a regulated way, through processes that ensure swift resolution of inflammation yet make provision for neutrophils to fulfill their microbicidal function. Phagocytic cells carry out this clearance by recogniz-

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Defects in intracellular oxidative metabolism of neutrophils undergoing apoptosis

Abstract: Abstract:Apoptosis permits neutrophil recognition by macrophages, thereby not only limiting potential cytotoxicity but also promoting resolution of inflammation.

Cited by 45 publications

References 47 publications

Phorbol Myristate Acetate Induces Neutrophil Death through Activation of p38 Mitogen-Activated Protein Kinase That Requires Endogenous Reactive Oxygen Species Other Than HOCl

Phorbol Myristate Acetate Induces Neutrophil Death through Activation of p38 Mitogen-Activated Protein Kinase That Requires Endogenous Reactive Oxygen Species Other Than HOCl

Activation of the granule pool of the NADPH oxidase accelerates apoptosis in human neutrophils

NADPH Oxidase-dependent Oxidation and Externalization of Phosphatidylserine during Apoptosis in Me2SO-differentiated HL-60 Cells

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