Different procedures of diphenyleneiodonium chloride addition affect neutrophil extracellular trap formation

Ostafin, Magdalena; Pruchniak, Michał Przemysław; Ciepiela, Olga; Reznick, Abraham Z.; Demkow, Urszula

doi:10.1016/j.ab.2016.05.003

Cited by 23 publications

(19 citation statements)

References 27 publications

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“…These findings confirmed that DPI is able to block NET creation. However, the addition of DPI together with PMA or the addition of inhibitor initially and then washing it out before stimulation resulted in different levels of NET formation [ 192 ]. These findings necessitate more studies to look into the mechanism of action of DPI under different conditions and in different diseases as a potential therapeutic for NETs.…”

Section: Potential Anti-net Therapeuticsmentioning

confidence: 99%

A Review of Neutrophil Extracellular Traps (NETs) in Disease: Potential Anti-NETs Therapeutics

Mutua

Gershwin

2020

Clinic Rev Allerg Immunol

341

248

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Activated neutrophils release neutrophil extracellular traps (NETs) in response to a variety of stimuli. NETosis is driven by protein-arginine deiminase type 4, with the release of intracellular granule components that function by capturing and destroying microbes, including viral, fungal, bacterial, and protozoal pathogens. The positive effects of pathogen control are countered by pro-inflammatory effects as demonstrated in a variety of diseases. Components of NETS are non-specific, and other than controlling microbes, they cause injury to surrounding tissue by themselves or by increasing the pro-inflammatory response. NETs can play a role in enhancement of the inflammation seen in autoimmune diseases including psoriasis, rheumatoid arthritis, and systemic lupus erythematosis. In addition, autoinflammatory diseases such as gout have been associated with NETosis. Inhibition of NETs may decrease the severity of many diseases improving survival. Herein, we describe NETosis in different diseases focusing on the detrimental effect of NETs and outline possible therapeutics that can be used to mitigate netosis. There is a need for more studies and clinical trials on these and other compounds that could prevent or destroy NETs, thereby decreasing damage to patients.

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Section: Potential Anti-net Therapeuticsmentioning

confidence: 99%

A Review of Neutrophil Extracellular Traps (NETs) in Disease: Potential Anti-NETs Therapeutics

Mutua

Gershwin

2020

Clinic Rev Allerg Immunol

341

248

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“…Accordingly, the problem of unspecific inhibition of various cell signaling pathways has been repeatedly brought up . Moreover, we and others have previously observed that slight modifications to experimental settings or conditions may lead to dissonant results . Therefore, the complexity of NETs formation mechanisms could be more easily studied if examined cells were amenable to genetic manipulations.…”

Section: Introductionmentioning

confidence: 99%

“…[16][17][18] Moreover, we and others have previously observed that slight modifications to experimental settings or conditions may lead to dissonant results. [18][19][20][21] Therefore, the complexity of NETs formation mechanisms could be more easily studied if examined cells were amenable to genetic manipulations. Since mature neutrophils cannot be subjected to genetic modifications using current techniques, 22 genetically modified neutrophil precursors (myelopoietic cells or cell lines), with silenced or overexpressed genes regulating various molecular pathways, should be implemented.…”

Section: Introductionmentioning

confidence: 99%

The influence of agents differentiating HL‐60 cells toward granulocyte‐like cells on their ability to release neutrophil extracellular traps

et al. 2018

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Studies on neutrophil extracellular traps (NETs) are challenging as neutrophils live shortly and easily become activated. Thus, availability of a cell line model closely resembling the functions of peripheral blood neutrophils would be advantageous. Our purpose was to find a compound that most effectively differentiates human promyelocytic leukemia (HL-60) cells toward granulocyte-like cells able to release NETs. HL-60 cells were differentiated with all-trans retinoic acid (ATRA), dimethyl sulfoxide (DMSO) or dimethylformamide (DMF) and stimulated with phorbol 12-myristate 13-acetate (PMA) or calcium ionophore A23187 (CI). Cell differentiation, phagocytosis and calcium influx were analyzed by flow cytometry. Reactive oxygen species production and NETs release were measured fluorometrically and analyzed microscopically. LC3-II accumulation and histone 3 citrullination were analyzed by western blot. ATRA most effectively differentiated HL-60 cells toward granulocyte-like cells. ATRA-dHL-60 cells released NETs only upon PMA stimulation, DMSO-dHL-60 cells only post CI stimulation, while DMF-dHL-60 cells formed NETs in response to both stimuli. Oxidative burst was induced in ATRA-, DMSO- and DMF-dHL-60 cells post PMA stimulation and only in DMF-dHL-60 cells post CI stimulation. Increased histone 3 citrullination was observed in stimulated DMSO- and DMF-, but not in ATRA-dHL-60 cells. The calcium influx was diminished in ATRA-dHL-60 cells. Significant increase in autophagosomes formation was observed only in PMA-stimulated DMF-dHL-60 cells. Phagocytic index was higher in ATRA-dHL-60 cells than in control, DMSO- and DMF-dHL-60 cells. We conclude that ATRA, DMSO and DMF differentiate HL-60 in different mechanisms. DMF is the best stimulus for HL-60 cell differentiation for NETs studies.

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“…As an inhibitor of NADPH oxidase, DPI acts differentially from APO and it decreases the amount of DNA in both SF and control cell types at 72 and 120 h, having a greater effect on SF cells, suggesting a cytolytic effect. In addition to its wide use as an inhibitor of NADPH oxidase, DPI has been reported to inhibit other important enzymes such as NADPH ubiquinone oxidoreductase, nitric oxide synthase, xanthine oxidase, NADPH cytochrome P450 oxidoreductase, and cholinesterase that may be involved in cell survival [34]. Apocynin however is a specific inhibitor of NADPH oxidase [35].…”

Section: Discussionmentioning

confidence: 99%

Reactive Oxygen Species from NADPH Oxidase and Mitochondria Participate in the Proliferation of Aortic Smooth Muscle Cells from a Model of Metabolic Syndrome

López-Acosta

Fortis-Barrera

Barrios-Maya

et al. 2018

Oxidative Medicine and Cellular Longevity

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In metabolic diseases, the increased reactive oxygen species (ROS) represents one of the pathogenic mechanisms for vascular disease probably by promoting vascular smooth muscle cell (SMC) proliferation that contributes to the development of arterial remodeling and stenosis, hypertension, and atherosclerosis. Therefore, this work was undertaken to evaluate the participation of ROS from NADPH oxidase and mitochondria in the proliferation of SMCs from the aorta in a model of metabolic syndrome induced by sucrose feeding in rats. After 24 weeks, sucrose-fed (SF) rats develop hypertension, intra-abdominal obesity, hyperinsulinemia, and hyperleptinemia. In addition SMCs from SF rats had a higher growth rate and produce more ROS than control cells. The treatment of SMCs with DPI and apocynin to inhibit NADPH oxidase and with tempol to scavenge superoxide anion significantly blocked the proliferation of both SF and control cells suggesting the participation of NADPH oxidase as a source of superoxide anion. MitoTEMPO, which targets mitochondria within the cell, also significantly inhibited the proliferation of SMCs having a greater effect on cells from SF than from the control aorta. The higher rate of cell growth from the SF aorta is supported by the increased content of cyclophilin A and CD147, proteins involved in the mechanism of cell proliferation. In addition, caldesmon, α-actin, and phosphorylated myosin light chain, contractile phenotype proteins, were found significantly lower in SF cells in no confluent state and increased in confluent state but without difference between both cell types. Our results suggest that ROS from NADPH oxidase and mitochondria significantly participate in the difference found in the rate of cell growth between SF and control cells.

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Different procedures of diphenyleneiodonium chloride addition affect neutrophil extracellular trap formation

Cited by 23 publications

References 27 publications

A Review of Neutrophil Extracellular Traps (NETs) in Disease: Potential Anti-NETs Therapeutics

A Review of Neutrophil Extracellular Traps (NETs) in Disease: Potential Anti-NETs Therapeutics

The influence of agents differentiating HL‐60 cells toward granulocyte‐like cells on their ability to release neutrophil extracellular traps

Reactive Oxygen Species from NADPH Oxidase and Mitochondria Participate in the Proliferation of Aortic Smooth Muscle Cells from a Model of Metabolic Syndrome

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