Evidence map›Paper›PMID 24599284›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2014

Rapid shedding of proinflammatory microparticles by human mononuclear cells exposed to cigarette smoke is dependent on Ca2+ mobilization.

Cinzia Cordazzo, Silvia Petrini, Tommaso Neri, Stefania Lombardi, Yuri Carmazzi, Roberto Pedrinelli, Pierluigi Paggiaro, Alessandro Celi

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed.

  1. Review
  2. Harmonising cellular conversations: decoding the vital roles of extracellular vesicles in respiratory system intercellular communications.European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  3. Review
  4. Epigenetic regulation of pulmonary inflammation.Seminars in cell & developmental biology · 2024
    Review
  5. Review
  6. Review
  7. Extracellular Vesicles as "Very Important Particles" (VIPs) in Aging.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Unravelling the mechanisms driving multimorbidity in COPD to develop holistic approaches to patient-centred care.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Cinzia CordazzoLaboratory of Respiratory Cell Biology, Dipartimento di Patologia Chirurgica, Medica, Molecolare e di Area Critica, University of Pisa and Azienda Ospedaliero-Universitaria Pisana, Ospedale di Cisanello, Via Paradisa, 2, 56124, Pisa, Italy.
Silvia Petrini
Tommaso Neri
Stefania Lombardi
Yuri Carmazzi
Roberto Pedrinelli
Pierluigi Paggiaro
Alessandro Celi

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesMicroparticles are membrane vesicles shed by cells upon activation and apoptosis. Agonists capable of inducing microparticle generation include cytokines, bacterial products, P-selectin, histamine. Cigarette smoke extract has also been recognized as an agonist involved in microparticle generation with an apoptosis-dependent mechanism. We investigated the possibility that cigarette smoke extract induces the rapid generation of proinflammatory microparticles by human mononuclear cells with a calcium-dependent mechanism. MATERIALS AND

methodsHuman mononuclear cells were exposed to cigarette smoke extract. [Ca(2+)]i mobilization was assessed with the fluorescent probe Fluo-4 NW. Microparticles were quantified with a prothrombinase assay and by flow cytometry. Normal human bronchial epithelial cells and A549 alveolar cells were incubated with cigarette smoke extract-induced microparticles and the generation of ICAM-1, IL-8, and MCP-1 was assessed by ELISA.

resultsExposure to cigarette smoke extract induced a rapid increase in [Ca(2+)]i mobilization. Microparticle generation was also increased. EGTA, verapamil and the calmodulin inhibitor, W-7, inhibited microparticle generation. Incubation of lung epithelial cells with cigarette smoke extract-induced microparticles increased the expression of proinflammatory mediators.

conclusionsExposure of mononuclear cells to cigarette smoke extract causes a rapid shedding of microparticles with a proinflammatory potential that might add to the mechanisms of disease from tobacco use.

Indexed as

SmokeApoptosisBronchiCalciumCell-Derived MicroparticlesCell Line, TumorCells, CulturedCell SurvivalChemokine CCL2Complex MixturesEpithelial CellsHumansIntercellular Adhesion Molecule-1Interleukin-8Leukocytes, MononuclearCalciumCCL2 protein, humanChemokine CCL2Complex MixturesCXCL8 protein, humanICAM1 protein, humanIntercellular Adhesion Molecule-1Interleukin-8Smoke

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Read underepoch 390

Registered trials

None linked

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.