ArticleThe Journal of biological chemistry2015
Factors Associated with Nitric Oxide-mediated β2 Integrin Inhibition of Neutrophils.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Allosteric Disulfide Bridges in Integrins: The Molecular Switches of Redox Regulation of Integrin-Mediated Cell Functions.Antioxidants (Basel, Switzerland) · 2025Review
- Inhaled nitric oxide suppresses neuroinflammation in experimental ischemic stroke.Journal of neuroinflammation · 2023Article
- Single-cell RNA-sequencing analysis of aortic valve interstitial cells demonstrates the regulation of integrin signaling by nitric oxide.Frontiers in cardiovascular medicine · 2022Article
- Effects of L-arginine on impaired blood fluidity after high-intensity exercise: An in vitro evaluation.Clinical hemorheology and microcirculation · 2022Article
- Role of NO and S-nitrosylation in the Expression of Endothelial Adhesion Proteins That Regulate Leukocyte and Tumor Cell Adhesion.Frontiers in physiology · 2020Review
- Local anaesthetics upregulate nitric oxide generation in cord blood and adult human neutrophils.Scientific reports · 2019Article
- Neutrophil microparticle production and inflammasome activation by hyperglycemia due to cytoskeletal instability.The Journal of biological chemistry · 2017Article
- Actin filaments-A target for redox regulation.Cytoskeleton (Hoboken, N.J.) · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This investigation explored the mechanism for inhibition of β2 integrin adhesion molecules when neutrophils are exposed to nitric oxide ((•)NO). Roles for specific proteins were elucidated using chemical inhibitors, depletion with small inhibitory RNA, and cells from knock-out mice. Optimal inhibition occurs with exposures to a (•)NO flux of ∼ 28 nmol/min for 2 min or more, which sets up an autocatalytic cascade triggered by activating type 2 nitric-oxide synthase (NOS-2) and NADPH oxidase (NOX). Integrin inhibition does not occur with neutrophils exposed to a NOX inhibitor (Nox2ds), a NOS-2 inhibitor (1400 W), or with cells from mice lacking NOS-2 or the gp91(phox) component of NOX. Reactive species cause S-nitrosylation of cytosolic actin that enhances actin polymerization. Protein cross-linking and actin filament formation assays indicate that increased polymerization occurs because of associations involving vasodilator-stimulated phosphoprotein, focal adhesion kinase, and protein-disulfide isomerase in proximity to actin filaments. These effects were inhibited in cells exposed to ultraviolet light which photo-reverses S-nitrosylated cysteine residues and by co-incubations with cytochalasin D. The autocatalytic cycle can be arrested by protein kinase G activated with 8-bromo-cyclic GMP and by a high (•)NO flux (∼ 112 nmol/min) that inactivates NOX.
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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.