Evidence map›Paper›PMID 9449721›Full record

ArticleThe Journal of experimental medicine1998

Disruption of fas receptor signaling by nitric oxide in eosinophils.

H Hebestreit, B Dibbert, I Balatti, D Braun, A Schapowal, K Blaser, H U Simon

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
13.6field-weighted citation impact, top 1% of its field
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

20 citing papers in PubMed, 176 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Mitochondria in the center of human eosinophil apoptosis and survival.International journal of molecular sciences · 2014
    Review
  10. Nitric oxide-induced apoptosis of human dental pulp cells is mediated by the mitochondria-dependent pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2014
    Article
  11. Review
  12. Article
  13. Human eosinophils release IL-1ß and increase expression of IL-17A in activated CD4+ T lymphocytes.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2012
    Article
  14. Article
  15. Article
  16. Article
  17. Eosinophil survival and apoptosis in health and disease.Allergy, asthma & immunology research · 2010
    Article
  18. Article
  19. Article
  20. Article
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

7 authors at 1 institution in 1 country.

H HebestreitSwiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, CH-7270 Davos, Switzerland.
B Dibbert
I Balatti
D Braun
A Schapowal
K Blaser
H U Simon
University of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been suggested that Fas ligand-Fas receptor interactions are involved in the regulation of eosinophil apoptosis and that dysfunctions in this system could contribute to the accumulation of these cells in allergic and asthmatic diseases. Here, we demonstrate that nitric oxide (NO) specifically prevents Fas receptor-mediated apoptosis in freshly isolated human eosinophils. In contrast, rapid acceleration of eosinophil apoptosis by activation of the Fas receptor occurs in the presence of eosinophil hematopoietins. Analysis of the intracellular mechanisms revealed that NO disrupts Fas receptor-mediated signaling events at the level of, or proximal to, Jun kinase (JNK), but distal to sphingomyelinase (SMase) activation and ceramide generation. In addition, activation of SMase occurs downstream of an interleukin 1 converting enzyme-like (ICE-like) protease(s) that is not blocked by NO. However, NO prevents activation of a protease that targets lamin B1. These findings suggest a role for an additional NO-sensitive apoptotic signaling pathway that amplifies the proteolytic cascade initialized by activation of the Fas receptor. Therefore, NO concentrations within allergic inflammatory sites may be important in determining whether an eosinophil survives or undergoes apoptosis upon Fas ligand stimulation.

Indexed as

ApoptosisCell SurvivalCoculture TechniquesEosinophilsFas Ligand ProteinFlow CytometryGene Expression Regulation, NeoplasticHistocytochemistryHumansImmunoblottingMembrane GlycoproteinsNasal PolypsNitric OxideNitric Oxide SynthaseRNASecond Messenger SystemsFASLG protein, humanFas Ligand ProteinMembrane GlycoproteinsNitric OxideNitric Oxide SynthaseRNA

Identifiers

PMID9449721
PMCPMC2212112
OpenAlexW2136790250

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.