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

Manda-Handzlik, Aneta; Bystrzycka, Weronika; Wachowska, Malgorzata; Sieczkowska, Sandra; Stelmaszczyk-Emmel, Anna; Demkow, Urszula; Ciepiela, Olga

doi:10.1111/imcb.12015

Cited by 49 publications

(52 citation statements)

References 46 publications

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“…HL-60 and r 0 cells were differ-N entiated into neutrophil-like cells by treatment with 1.25% dimethyl sulfoxide (DMSO) or 1 mM all-trans retinoic acid (ATRA) for 3 days, as described previously. (13) Quantification of extracellular DNA. Neutrophil-like HL-60 and r 0 cells pretreated with or without 4-aminobenzoic acid hydrazide (ABAH; MPO inhibitor) for 3 h, MitoTEMPO (mitochondrial ROS scavenger) for 30 min, or necrosulfonamide [NSA; mixed lineage kinase domain like psedokinase (MLKL) inhibitor] for 30 min were seeded at 1´10 6 cell/ml in 96-well plates.…”

Section: Methodsmentioning

confidence: 99%

Formation of neutrophil extracellular traps in mitochondrial DNA-deficient cells

Takishita

Yasuda

Shimizu

et al. 2020

J. Clin. Biochem. Nutr.

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Neutrophil extracellular trap (NET) formation plays an important role in inflammatory diseases. Although it is known that NET formation occurs via NADPH oxidase (NOX) dependent and NOX independent pathways, the detailed mechanism remains unknown. Therefore, in this study, we aimed to elucidate the role of mito chondria in NOX dependent and NOX independent NET formation. We generated mitochondrial DNA deficient cells (ρ 0 cells) by treating HL 60 cells with dideoxycytidine and differentiated them to neutrophil like cells. These neutrophil like ρ 0 cells showed markedly reduced NOX independent NET formation but not NOX dependent NET formation. However, NET associated intracellular histone citrullination was not inhibited in ρ 0 cells. Furthermore, cells membrane disruption in NOX dependent NET formation occurred in a Myeloperoxidase (MPO) and mixed lineage kinase domain like pseudokinase (MLKL) dependent manner; however, cell membrane disruption in NOX independent NET formation partially occurred in an MLKL dependent manner. These results highlight the importance of mitochondria in NOX independent NET formation.

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Section: Methodsmentioning

confidence: 99%

Formation of neutrophil extracellular traps in mitochondrial DNA-deficient cells

Takishita

Yasuda

Shimizu

et al. 2020

J. Clin. Biochem. Nutr.

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“…HL-60 cell culture propagation and differentiation with dimethylformamide (DMF) into granulocyte-like cells were performed exactly as described previously [18].…”

Section: Sources Of Granulocytes and Granulocyte-like Cellsmentioning

confidence: 99%

Nitric oxide and peroxynitrite trigger and enhance release of neutrophil extracellular traps

Manda-Handzlik

Bystrzycka

Cieloch

et al. 2019

Cell. Mol. Life Sci.

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Despite great interest, the mechanism of neutrophil extracellular traps (NETs) release is not fully understood and some aspects of this process, e.g. the role of reactive nitrogen species (RNS), still remain unclear. Therefore, our aim was to investigate the mechanisms underlying RNS-induced formation of NETs and contribution of RNS to NETs release triggered by various physiological and synthetic stimuli. The involvement of RNS in NETs formation was studied in primary human neutrophils and differentiated human promyelocytic leukemia cells (HL-60 cells). RNS (peroxynitrite and nitric oxide) efficiently induced NETs release and potentiated NETs-inducing properties of platelet activating factor and lipopolysaccharide. RNS-induced NETs formation was independent of autophagy and histone citrullination, but dependent on the activity of phosphoinositide 3-kinases (PI3K) and myeloperoxidase, as well as selective degradation of histones H2A and H2B by neutrophil elastase. Additionally, NADPH oxidase activity was required to release NETs upon stimulation with NO, as shown in NADPH-deficient neutrophils isolated from patients with chronic granulomatous disease. The role of RNS was further supported by increased RNS synthesis upon stimulation of NETs release with phorbol 12-myristate 13-acetate and calcium ionophore A23187. Scavenging or inhibition of RNS formation diminished NETs release triggered by these stimuli while scavenging of peroxynitrite inhibited NO-induced NETs formation. Our data suggest that RNS may act as mediators and inducers of NETs release. These processes are PI3K-dependent and ROS-dependent. Since inflammatory reactions are often accompanied by nitrosative stress and NETs formation, our studies shed a new light on possible mechanisms engaged in various immune-mediated conditions. Keywords Autophagy • Neutrophil extracellular traps • Nitric oxide • Peroxynitrite • Phosphoinositide 3-kinases • Reactive nitrogen species Abbreviations 3-MA 3-Methyladenine ABAH Aminobenzoic acid hydrazide AKT Protein kinase B CGD Chronic granulomatous disease CI Calcium ionophore A23187 DHR 123 Dihydrorhodamine 123 DPI Diphenyleneiodonium ERK Extracellular signal-regulated kinases IL Interleukin LC3 protein Light chain 3 protein L-NAME N-nitroarginine methyl ester LPS Lipopolysaccharide MAPK Mitogen-activated protein kinases MPO Myeloperoxidase NAC N-acetylcysteine NE Neutrophil elastase NEi Neutrophil elastase inhibitor GW 311616A NETs Neutrophil extracellular traps NBT Nitroblue tetrazolium NO Nitric oxide NOS Nitric oxide synthase Cellular and Molecular Life Sciences Malgorzata Wachowska and Urszula Demkow have contributed equally.

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“…The HL-60 cells cultured in 10% FBS medium were treated with DMSO (1.25%) to induce the differentiation into neutrophil-like cells [18]. After five days, the cells were stimulated with PMA (MedChemExpress, Monmouth Junction, NJ, USA) (100 ng/ml, dissolved in DMSO) or medium or DMSO.…”

Section: In Vitro Experimentsmentioning

confidence: 99%

Three Ingredients of Safflower Alleviate Acute Lung Injury and Inhibit NET Release Induced by Lipopolysaccharide

Wang

Guo

Wen

et al. 2020

Mediators of Inflammation

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Xuebijing injection is a Chinese herb compound to treat sepsis in China, but it contains many different kinds of components, and each component may have different effects in treating sepsis. The present study was performed to investigate the effect of three ingredients of Xuebijing, safflor yellow A (SYA), hydroxysafflor yellow A (HSYA), and anhydrosafflor yellow B (AHSYB), in lipopolysaccharide- (LPS-) induced acute lung injury (ALI). LPS (10 mg/kg) was injected intratracheally to induce acute lung injury in mice, which were then treated with SYA, HSYA, and AHSYB. The blood, bronchoalveolar lavage fluid (BALF), and lung tissues were collected to detect degree of lung injury, level of inflammation, and neutrophil extracellular traps (NETs). In vitro experiments were performed using HL-60 cells stimulated with phorbol myristate acetate (PMA). Lung injury induced by LPS was alleviated by SYA, HSYA, and AHSYB as demonstrated by the histopathologic test. The three components inhibit LPS-induced elevation of the levels of inflammatory factors and wet-to-dry weight ratio as well as the amount of protein and cells in the BALF. They also induced a remarkably less overlay of myeloperoxidase (MPO) and histone in the immunofluorescence assay and reduced level of MPO-DNA complex in plasma. The in vitro assay showed a similar trend that the three components inhibited PMA-induced NET release in neutrophil-like HL-60 cells. Western blot demonstrated that phosphorylation of c-rapidly accelerated fibrosarcoma (c-Raf), mitogen-activated protein kinase ERK kinase (MEK), and extracellular signal-regulated kinase (ERK) in the lungs of LPS-challenged mice, and PMA-treated HL-60 cells were all significantly reduced by SYA, HSYA, and AHSYB. Therefore, our data demonstrated that three components of XBJ, including SYA, HSYA, and AHSYB, showed a protective effect against LPS-induced lung injury and NET release.

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

Cited by 49 publications

References 46 publications

Formation of neutrophil extracellular traps in mitochondrial DNA-deficient cells

Formation of neutrophil extracellular traps in mitochondrial DNA-deficient cells

Nitric oxide and peroxynitrite trigger and enhance release of neutrophil extracellular traps

Three Ingredients of Safflower Alleviate Acute Lung Injury and Inhibit NET Release Induced by Lipopolysaccharide

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