ArticleThe Journal of biological chemistry2012
Stimulation of unprimed macrophages with immune complexes triggers a low output of nitric oxide by calcium-dependent neuronal nitric-oxide synthase.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 54 citations in OpenAlex.
- S-nitrosylation of IRF7 induced by NOS1 expression in melanoma suppresses anti-tumor immunity.Cell death & disease · 2026Article
- Effects of Akt Activator SC79 on Human M0 Macrophage Phagocytosis and Cytokine Production.Cells · 2024Article
- Daidzein and Equol: Ex Vivo and In Silico Approaches Targeting COX-2, iNOS, and the Canonical Inflammasome Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Monocytes from Uninfected Neonates Born toPathogens (Basel, Switzerland) · 2023Article
- Effect of electroacupuncture on haemodynamic changes during intubation for general anaesthesia is mediated by nitric oxide synthase‑3 via the regulation of microRNA‑155, microRNA‑335 and microRNA‑383.Molecular medicine reports · 2023Article
- Macrophage Polarization and Reprogramming in Acute Inflammation: A Redox Perspective.Antioxidants (Basel, Switzerland) · 2022Review
- Article
- Bitter taste receptors stimulate phagocytosis in human macrophages through calcium, nitric oxide, and cyclic-GMP signaling.Cellular and molecular life sciences : CMLS · 2021Article
- Nitric oxide in cellular adaptation and disease.Redox biology · 2020Review
- Molecular Mechanisms by Which Selenoprotein K Regulates Immunity and Cancer.Biological trace element research · 2019Review
- Progress in the emerging role of selenoproteins in cardiovascular disease: focus on endoplasmic reticulum-resident selenoproteins.Cellular and molecular life sciences : CMLS · 2019Review
- Shape of ligand immobilized particles dominates and amplifies the macrophage cytokine response to ligands.PloS one · 2019Article
- Selenoprotein K Increases Efficiency of DHHC6 Catalyzed Protein Palmitoylation by Stabilizing the Acyl-DHHC6 Intermediate.Antioxidants (Basel, Switzerland) · 2017Article
- The TLR4-NOS1-AP1 signaling axis regulates macrophage polarization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Article
- Inducible Nitric Oxide Synthase (iNOS) Is a Novel Negative Regulator of Hematopoietic Stem/Progenitor Cell Trafficking.Stem cell reviews and reports · 2017Article
- Selenoprotein K regulation of palmitoylation and calpain cleavage of ASAP2 is required for efficient FcγR-mediated phagocytosis.Journal of leukocyte biology · 2017Article
- Exogenous l-Valine Promotes Phagocytosis to Kill Multidrug-Resistant Bacterial Pathogens.Frontiers in immunology · 2017Article
- A Nanoparticle-based Sensor Platform for Cell Tracking and Status/Function Assessment.Scientific reports · 2015Article
- Selenoprotein K and protein palmitoylation.Antioxidants & redox signaling · 2015Review
- NOS1-derived nitric oxide promotes NF-κB transcriptional activity through inhibition of suppressor of cytokine signaling-1.The Journal of experimental medicine · 2015Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Immune complexes composed of IgG-opsonized pathogens, particles, or proteins are phagocytosed by macrophages through Fcγ receptors (FcγRs). Macrophages primed with IFNγ or other pro-inflammatory mediators respond to FcγR engagement by secreting high levels of cytokines and nitric oxide (NO). We found that unprimed macrophages produced lower levels of NO, which required efficient calcium (Ca(2+)) flux as demonstrated by using macrophages lacking selenoprotein K, which is required for FcγR-induced Ca(2+) flux. Thus, we further investigated the signaling pathways involved in low output NO and its functional significance. Evaluation of inducible, endothelial, and neuronal nitric-oxide synthases (iNOS, eNOS, and nNOS) revealed that FcγR stimulation in unprimed macrophages caused a marked Ca(2+)-dependent increase in both total and phosphorylated nNOS and slightly elevated levels of phosphorylated eNOS. Also activated were three MAP kinases, ERK, JNK, and p38, of which ERK activation was highly dependent on Ca(2+) flux. Inhibition of ERK reduced both nNOS activation and NO secretion. Finally, Transwell experiments showed that FcγR-induced NO functioned to increase the phagocytic capacity of other macrophages and required both NOS and ERK activity. The production of NO by macrophages is conventionally attributed to iNOS, but we have revealed an iNOS-independent receptor/enzyme system in unprimed macrophages that produces low output NO. Under these conditions, FcγR engagement relies on Ca(2+)-dependent ERK phosphorylation, which in turn increases nNOS and, to a lesser extent, eNOS, both of which produce low levels of NO that function to promote phagocytosis.
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Registered trials
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.