ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2009
Effects of exogenous annexin-1 on lipopolysaccharide-induced proliferation and reactive oxygen species production partially through modulation of CRAC channels but independent of NF-kappaB pathway.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Annexin-1 Mimetic Peptide Ac2-26 Suppresses Inflammatory Mediators in LPS-Induced Astrocytes and Ameliorates Pain Hypersensitivity in a Rat Model of Inflammatory Pain.Cellular and molecular neurobiology · 2020Article
- Cathepsin G-regulated release of formyl peptide receptor agonists modulate neutrophil effector functions.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the effects of exogenous annexin-1 (ANXA1) on lipopolysaccharide(LPS)-induced proliferation, reactive oxygen species (ROS) production, and calcium signal transduction in RAW264.7 macrophages.
methodsRAW264.7 macrophages were treated with or without LPS in the absence or presence of ANXA1. The proliferation effects were detected by Cell Counting Kit-8 assay. ROS were quantified by flow cytometry and fluorescence microscopy. Intracellular Ca(2+) concentration ([Ca(2+)](i)) was analyzed by laser confocal scanning microscopy. IkappaBalpha degradation and NF-kappaB translocation were tested by Western blot.
resultsExogenous ANXA1 inhibited LPS-induced proliferation and ROS production in a dose-dependent manner. LPS evoked [Ca(2+)](i) increase through CRAC channels, and ANXA1 suppressed LPS-induced [Ca(2+)](i) increase in a dose-dependent manner. The CRAC channels were associated with LPS-induced proliferation and ROS production. Exogenous ANXA1 had no effect on LPS-induced IkappaB degradation and NF-kappaB translocation.
conclusionsANXA1 inhibited LPS-induced proliferation and ROS production in RAW264.7 macrophages partially through modulation of CRAC channels but independent of the NF-kappaB pathway.
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19685206What OpenQuestion holds
Registered trials
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