NADPH Oxidase-Dependent Production of Reactive Oxygen Species Induces Endoplasmatic Reticulum Stress in Neutrophil-Like HL60 Cells

Kuwabara, Wilson Mitsuo Tatagiba; Zhang, Liling; Schuiki, Irmgard; Curi, Rui; Volchuk, Allen; Alba-Loureiro, Tatiana Carolina

doi:10.1371/journal.pone.0116410

Cited by 58 publications

(37 citation statements)

References 75 publications

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“…8c, e ) and others study suggests an increase in NO and ROS production in monocytes (primary response) and differentiated macrophage (Fig. 8d secondary response) in response to LPS and PMA 40 , 41 , . Interestingly, NADH-THP-1, ADH-THP-1, and adhered PBMC all of them show enhanced production of NO and ROS, in response to covering with agarose gel.…”

Section: Resultssupporting

confidence: 51%

3D micro-environment regulates NF-κβ dependent adhesion to induce monocyte differentiation

et al. 2018

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Differentiation of monocytes entails their relocation from blood to the tissue, hence accompanied by an altered physicochemical micro-environment. While the mechanism by which the biochemical make-up of the micro-environment induces differentiation is known, the fluid-like to gel-like transition in the physical micro-environment is not well understood. Monocytes maintain non-adherent state to prevent differentiation. We establish that irrespective of the chemical makeup, a 3D gel-like micro-environment induces a positive-feedback loop of adhesion-MAPK-NF-κβ activation to facilitate differentiation. In 2D fluid-like micro-environment, adhesion alone is capable of inducing differentiation via the same positive-feedback signaling. Chemical inducer treatment in fluid-like micro-environment, increases the propensity of monocyte adhesion via a brief pulse of p-MAPK. The adhesion subsequently elicit differentiation, establishing that adhesion is both necessary and sufficient to induce differentiation in 2D/3D micro-environment. MAPK, and NF-κβ being key molecules of multiple signaling pathways, we hypothesize that biochemically inert 3D gel-like micro-environment would also influence other cellular functions.

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Section: Resultssupporting

confidence: 51%

3D micro-environment regulates NF-κβ dependent adhesion to induce monocyte differentiation

et al. 2018

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“…However, glucose has limited entry into leukocytes since these cells present the glucose transporter 1 (GLUT1). GLUT1 has low K m (1–2 mM), and so, once the transport is saturated, there is no further glucose entry into the cells despite its levels increase in plasma (67). …”

Section: Discussionmentioning

confidence: 99%

Autophagy Is Impaired in Neutrophils from Streptozotocin-Induced Diabetic Rats

2017

Self Cite

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We tested the hypothesis that changes reported on functions of neutrophils from streptozotocin-induced diabetic rats involve autophagy impairment. Wistar rats were rendered diabetic by streptozotocin injection (65 mg/kg, i.v.), and the measurements were carried out 2 weeks afterward. Neutrophils were collected through intraperitoneal cavity lavage after 4 h of i.p. oyster glycogen type 2 injection. Neutrophils cultured with PMA (20 nM) for 1 h were used for analysis of plasma membrane integrity, DNA fragmentation, and mitochondrial depolarization by flow cytometry; expression of Atg5, Atg14, Beclin1, LC3BII, and Rab9 by RT-PCR; the contents of caspase 3, LC3BII/LC3BI, and pS6 by western blotting; ATP content by fluorescence essay; reactive oxygen species production by chemiluminescence (Luminol), and autophagy by immunofluorescence tracking LC3B cleavage. Herein, neutrophils from diabetic rats had high DNA fragmentation, depolarization of mitochondrial membrane, low content of ATP, and high content of cleaved caspase 3 after PMA stimulation. Neutrophils from diabetic rats also had low expression of LC3B, failed to increase the expression of Rab9 and Atg14 induced by PMA stimulation. Neutrophils from diabetic animals also had low cleavage of LC3BI to LC3BII and do not present punctate structures that label autophagosomal membranes after stimulus. The changes of neutrophil function reported in diabetic rats do involve impaired autophagy. The suppression of autophagy in neutrophils from diabetic rats may be associated with the activation of the mTOR signaling as indicated by the high content of pS6.

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“…Considering these indicative markers of oxidative stress, tempol improved Hcy-induced endothelium-dependent vasodilatory impairment, indicating that ROS might be involved in Hcy-induced endothelium damage. A major source and modulatory enzyme of ROS in the vasculature was NADPH oxidase, a multisubunit enzyme which was composed of membrane-associated cytochrome b558 including p22phox and gp91phox subunits and cytoplasmic subunits including p47phox, p67phox, p40phox, and the small G protein Rac [ 22 ]. To exactly explore whether NADPH oxidase derived ROS played a role, apocynin, an NADPH oxidase inhibitor, was applied [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of Huang Qi Decoction on Endothelial Dysfunction Induced by Homocysteine

Chu

Mao

Wang

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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Vascular endothelial dysfunction can be induced by homocysteine (Hcy) through promoted oxidative stress. Huang Qi decoction (HQD) is a traditional Chinese medical formula and its components possess antioxidant effect. The study herein was therefore designed to investigate the effects of HQD at different dosage on endothelial dysfunction induced by Hcy. Tempol and apocynin were used to investigate whether antioxidant mechanisms were involved. Endothelium-dependent relaxation of rat aortas was investigated by isometric tension recordings. Reactive oxygen species (ROS) in human umbilical vein endothelial cells (HUVECs) was determined by DHE staining. The assessment related to oxidative stress and NO bioavailability was performed by assay kits and western blot. In isometric tension experiment, HQD at the dose of 30 or 100 μg/mL, tempol, or apocynin prevented impaired endothelium-dependent relaxation in isolated aortas elicited by Hcy. In cellular experiments, substantial enhancement in NADPH oxidase and ROS generation and reduction in NO bioavailability triggered by Hcy were reversed by pretreatment of HQD at the dose of 100 μg/mL, tempol, or apocynin. The results proved that HQD at an appropriate dosage presented favorable effects on endothelial dysfunction initiated by Hcy through antioxidant mechanisms. HQD can act as a potent prescription for the treatment of endothelium related vascular complications.

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NADPH Oxidase-Dependent Production of Reactive Oxygen Species Induces Endoplasmatic Reticulum Stress in Neutrophil-Like HL60 Cells

Cited by 58 publications

References 75 publications

3D micro-environment regulates NF-κβ dependent adhesion to induce monocyte differentiation

3D micro-environment regulates NF-κβ dependent adhesion to induce monocyte differentiation

Autophagy Is Impaired in Neutrophils from Streptozotocin-Induced Diabetic Rats

Effects of Huang Qi Decoction on Endothelial Dysfunction Induced by Homocysteine

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