ArticleClinical and experimental immunology2003
Calcium signalling is altered in myeloid cells with a deficiency in NADPH oxidase activity.
Article in Clinical and experimental immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 40 citations in OpenAlex.
- The Nox2 NADPH oxidase regulates neutrophilic inflammation in the oral cavity.Mucosal immunology · 2026Article
- Molecular regulation of neutrophil swarming in health and disease: Lessons from the phagocyte oxidase.iScience · 2023Review
- Article
- The intimate and controversial relationship between voltage-gated proton channels and the phagocyte NADPH oxidase.Immunological reviews · 2016Review
- Impact of reactive oxygen species (ROS) on the control of parasite loads and inflammation in Leishmania amazonensis infection.Parasites & vectors · 2016Article
- Dysregulated Ca2+ homeostasis in Fanconi anemia cells.Scientific reports · 2015Article
- NLRP3 inflammasome activation and interleukin-1β release in macrophages require calcium but are independent of calcium-activated NADPH oxidases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- New insights into the regulation of neutrophil NADPH oxidase activity in the phagosome: a focus on the role of lipid and Ca(2+) signaling.Antioxidants & redox signaling · 2013Review
- VSOP/Hv1 proton channels sustain calcium entry, neutrophil migration, and superoxide production by limiting cell depolarization and acidification.The Journal of experimental medicine · 2010Article
- Protein kinase C promotes restoration of calcium homeostasis to platelet activating factor-stimulated human neutrophils by inhibition of phospholipase C.Journal of inflammation (London, England) · 2009Article
- Pharmacological control of neutrophil-mediated inflammation: strategies targeting calcium handling by activated polymorphonuclear leukocytes.Drug design, development and therapy · 2009Article
- Regulation of superoxide production in neutrophils: role of calcium influx.Journal of leukocyte biology · 2008Review
- Role of Nox2 in elimination of microorganisms.Seminars in immunopathology · 2008Review
- Hyperinflammation in chronic granulomatous disease and anti-inflammatory role of the phagocyte NADPH oxidase.Seminars in immunopathology · 2008Review
- Hydrogen peroxide activates calcium influx in human neutrophils.Molecular and cellular biochemistry · 2008Article
- Consequences of the electrogenic function of the phagocytic NADPH oxidase.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2005Review
- Aberrant [correction of Abberant] cytosolic calcium ion mobilization in chronic granulomatous disease neutrophils.Inflammation · 2004Article
- Itraconazole antagonizes store-operated influx of calcium into chemoattractant-activated human neutrophils.Clinical and experimental immunology · 2004Article
- Holding back neutrophil aggression; the oxidase has potential.Clinical and experimental immunology · 2003Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The relation of O(2.-)-production and Ca2+ homeostasis was investigated in PLB-985 cell lines and neutrophilic granulocytes from peripheral blood. In differentiated wild-type PLB-985 cells, a high level of O(2.-)-production was associated with a significant decrease in the membrane potential and the inhibition of capacitative Ca2+ entry. These correlations were not observed in gp91phox -/- cells or in cells transfected with a non-functional mutant of gp91phox (Thr341Lys). Membrane depolarization and inhibition of Ca2+ entry reappeared in cells transfected with wild-type gp91phox. These experiments demonstrate that inhibition of Ca2+ entry depends on the presence of a functional NADPH oxidase. The Ca2+ signal induced by stimulation of chemotactic receptors also showed remarkable differences: [Ca2+]ic in the sustained phase was higher in gp91phox-/- than in wild-type cells. Alteration of the Ca2+ signal was reproduced by treating peripheral blood neutrophils with the NADPH oxidase inhibitor diphenylene-iodonium. It is concluded that the deficiency in O(2.-)-production is accompanied by significant alterations of Ca2+ homeostasis in myeloid cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.