ArticleThe Journal of biological chemistry2014
Neutrophils generate microparticles during exposure to inert gases due to cytoskeletal oxidative stress.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Varying Oxygen Partial Pressure Elicits Blood-Borne Microparticles Expressing Different Cell-Specific Proteins-Toward a Targeted Use of Oxygen?International journal of molecular sciences · 2022Trial
- Therapeutic Potential of GYY4137 in Reducing Oxidative Stress and Mortality in Experimental Decompression Sickness.Scientific reports · 2026Article
- A gradient-based optimization model for predicting decompression sickness risk.Frontiers in physiology · 2026Article
- Redox and actin, a fascinating story.Redox biology · 2025Review
- Metabolic landscape in venous thrombosis: insights into molecular biology and therapeutic implications.Annals of medicine · 2024Review
- Recombinant human plasma gelsolin suppresses persistent neuroinflammation and restores hippocampal neurogenesis in murine model of decompression sickness.Journal of neurophysiology · 2024Article
- A review of nutritional recommendations for scuba divers.Journal of the International Society of Sports Nutrition · 2024Review
- Inert Gas Mild Pressure Action on Healthy Humans: The "IPA" Study.International journal of molecular sciences · 2024Article
- Influence of exposure duration on human pressure-induced inflammatory responses: Comparison between tunnel workers and underwater divers.Physiological reports · 2024Article
- Gene expression of Decompression Sickness-resistant rats through a miRnome/transcriptome crossed approach.Communications biology · 2024Article
- Dissolved gases from pressure changes in the lungs elicit an immune response in human peripheral blood.Bioengineering & translational medicine · 2024Article
- Persistent neuroinflammation and functional deficits in a murine model of decompression sickness.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Microparticles in Human Perspiration as an Inflammatory Response Index.Diagnostics (Basel, Switzerland) · 2024Article
- Decompression illness: a comprehensive overview.Diving and hyperbaric medicine · 2024Article
- Extracellular microvesicles: biologic properties, biogenesis, and applications in leukemia.Molecular and cellular biochemistry · 2024Review
- Dissolved gases from pressure changes in the lungs elicit an immune response in human peripheral blood.bioRxiv : the preprint server for biology · 2023Article
- Elevations of Extracellular Vesicles and Inflammatory Biomarkers in Closed Circuit SCUBA Divers.International journal of molecular sciences · 2023Article
- Neuroinflammation with increased glymphatic flow in a murine model of decompression sickness.Journal of neurophysiology · 2023Article
- The Role of Platelet-Derived Extracellular Vesicles in Immune-Mediated Thrombosis.International journal of molecular sciences · 2022Review
- Extracellular Vesicles in Redox Signaling and Metabolic Regulation in Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This investigation was to elucidate the mechanism for microparticle (MP) formation triggered by exposures to high pressure inert gases. Human neutrophils generate MPs at a threshold of ∼186 kilopascals with exposures of 30 min or more. Murine cells are similar, but MP production occurs at a slower rate and continues for ∼4 h, whether or not cells remain under pressure. Neutrophils exposed to elevated gas but not hydrostatic pressure produce MPs according to the potency series: argon ≃ nitrogen > helium. Following a similar pattern, gases activate type-2 nitric-oxide synthase (NOS-2) and NADPH oxidase (NOX). MP production does not occur with neutrophils exposed to a NOX inhibitor (Nox2ds) or a NOS-2 inhibitor (1400W) or with cells from mice lacking NOS-2. Reactive species cause S-nitrosylation of cytosolic actin that enhances actin polymerization. Protein cross-linking and immunoprecipitation studies indicate that increased polymerization occurs because of associations involving vasodilator-stimulated phosphoprotein, focal adhesion kinase, the H(+)/K(+) ATPase β (flippase), the hematopoietic cell multidrug resistance protein ABC transporter (floppase), and protein-disulfide isomerase in proximity to short actin filaments. Using chemical inhibitors or reducing cell concentrations of any of these proteins with small inhibitory RNA abrogates NOS-2 activation, reactive species generation, actin polymerization, and MP production. These effects were also inhibited in cells exposed to UV light, which photoreverses S-nitrosylated cysteine residues and by co-incubations with the antioxidant ebselen or cytochalasin D. The autocatalytic cycle of protein activation is initiated by inert gas-mediated singlet O2 production.
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