ArticleThe Journal of biological chemistry2010
Myeloperoxidase-dependent inactivation of surfactant protein D in vitro and in vivo.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Revisiting surfactant protein D: an immune surveillance molecule bridging innate and adaptive immunity.Frontiers in immunology · 2024Review
- Association of genetic variations in ACE2, TIRAP and factor X with outcomes in COVID-19.PloS one · 2022Article
- Host factors: Implications in immunopathogenesis of COVID-19.Pathology, research and practice · 2021Review
- Halogen-Induced Chemical Injury to the Mammalian Cardiopulmonary Systems.Physiology (Bethesda, Md.) · 2021Review
- Article
- Cellular and Humoral Immune Responses in Covid-19 and Immunotherapeutic Approaches.ImmunoTargets and therapy · 2021Review
- Toll-like receptors and COVID-19: a two-faced story with an exciting ending.Future science OA · 2020Article
- Oxidative damage of SP-D abolishes control of eosinophil extracellular DNA trap formation.Journal of leukocyte biology · 2018Article
- Surfactant Protein D in Respiratory and Non-Respiratory Diseases.Frontiers in medicine · 2018Review
- Chlorine-induced cardiopulmonary injury.Annals of the New York Academy of Sciences · 2016Review
- Acute chlorine gas exposure produces transient inflammation and a progressive alteration in surfactant composition with accompanying mechanical dysfunction.Toxicology and applied pharmacology · 2014Article
- Air pollution and type 2 diabetes: mechanistic insights.Diabetes · 2012Review
- Increased surfactant protein D fails to improve bacterial clearance and inflammation in serpinB1-/- mice.American journal of respiratory cell and molecular biology · 2012Article
- S-nitrosylation of surfactant protein D as a modulator of pulmonary inflammation.Biochimica et biophysica acta · 2012Review
- Regulation of alveolar epithelial Na+ channels by ERK1/2 in chlorine-breathing mice.American journal of respiratory cell and molecular biology · 2012Article
- Myeloperoxidase targets apolipoprotein A-I, the major high density lipoprotein protein, for site-specific oxidation in human atherosclerotic lesions.The Journal of biological chemistry · 2012Article
- Chlorine gas exposure causes systemic endothelial dysfunction by inhibiting endothelial nitric oxide synthase-dependent signaling.American journal of respiratory cell and molecular biology · 2011Article
- Postexposure administration of a {beta}2-agonist decreases chlorine-induced airway hyperreactivity in mice.American journal of respiratory cell and molecular biology · 2011Article
- Segmental allergen challenge alters multimeric structure and function of surfactant protein D in humans.American journal of respiratory and critical care medicine · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Surfactant protein D (SP-D) plays diverse and important roles in innate immunity and pulmonary homeostasis. Neutrophils and myeloperoxidase (MPO) colocalized with SP-D in a murine bacterial pneumonia model of acute inflammation, suggesting that MPO-derived reactive species might alter the function of SP-D. Exposure of SP-D to the complete MPO-H(2)O(2)-halide system caused loss of SP-D-dependent aggregating activity. Hypochlorous acid (HOCl), the major oxidant generated by MPO, caused a similar loss of aggregating activity, which was accompanied by the generation of abnormal disulfide-cross-linked oligomers. A full-length SP-D mutant lacking N-terminal cysteine residues and truncation mutants lacking the N-terminal domains were resistant to the oxidant-induced alterations in disulfide bonding. Mass spectroscopy of HOCl-treated human SP-D demonstrated several modifications, but none involved key ligand binding residues. There was detectable oxidation of cysteine 15, but no HOCl-induced cysteine modifications were observed in the C-terminal lectin domain. Together, the findings localize abnormal disulfide cross-links to the N-terminal domain. MPO-deficient mice showed decreased cross-linking of SP-D and increased SP-D-dependent aggregating activity in the pneumonia model. Thus, MPO-derived oxidants can lead to modifications of SP-D structure with associated alterations in its characteristic aggregating activity.
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What OpenQuestion holds
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.