ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2010
Calcium pyrophosphate dihydrate crystal-induced inhibition of neutrophil apoptosis: involvement of Bcl-2 family members.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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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
3 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Systematic Overview of Solid Particles and Their Host Responses.Frontiers in immunology · 2018Pooled it
- Crystals, inflammation, and osteoarthritis.Current opinion in rheumatology · 2011Review
- Pathophysiology of articular chondrocalcinosis--role of ANKH.Nature reviews. Rheumatology · 2011Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
introductionThe inflammation associated with calcium pyrophosphate dihydrate (CPPD) crystal-induced arthritis arises from the activation of neutrophils with crystals in the synovial joint. Furthermore, constitutive neutrophil apoptosis is inhibited by this interaction with CPPD so that the lifetime of the cells and the duration of the inflammatory response are extended. The objective of this study was to investigate the role of bcl-2 protein family members in the CPPD-induced prosurvival response.
methodsApoptosis was measured using DNA fragmentation and Caspase 3 assays. The expression and activation levels of the bcl-2 protein family members A1, Mcl-1, Bcl-xl, Bim, Bad and Bax-alpha were measured using western blot analysis.
resultsThe prosurvival proteins Mcl-1 and Bcl-xl were both found to be strongly expressed but unaffected by CPPD-induced neutrophil activation over 3 h. The expression of proapoptotic proteins Bim and Bax-alpha was found to decrease over the time course of a 3 h incubation of neutrophils with CPPD crystals (but not the bacterial chemoattractant fMLP). Furthermore, expression of the unphosphorylated (active, proapoptotic) form of Bim was dominant in control cells at 0.5 h, whereas the status of this protein switched to the phosphorylated form following cell activation by both CPPD and fMLP. For CPPD (but not fMLP) this phosphorylation effect reversed over a 3 h incubation.
conclusionUpon stimulation by CPPD crystals, the expression of both Bim and Bax-alpha decreased after 3 h suggesting a reduced proapoptotic effect of these proteins so that the static expression of the prosurvival proteins Bcl-xl and Mcl-1 might allow for a temporary shift in the balance to a prosurvival state of the cells. Because a sudden (but transient) increase in the phosphorylated form of Bim was observed in CPPD-stimulated neutrophils it is possible that this species might act as a signaling intermediate, resulting in the observed downregulation of Bax-alpha.
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Registered trials
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