Evidence map›Paper›PMID 8394015›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1993

Transmembrane signaling in human polymorphonuclear neutrophils: 15(S)-hydroxy-(5Z,8Z,11Z,13E)-eicosatetraenoic acid modulates receptor agonist-triggered cell activation.

R J Smith, J M Justen, E G Nidy, L M Sam, J E Bleasdale

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Role of oxylipins in cardiovascular diseases.Acta pharmacologica Sinica · 2018
    Review
  6. Anti-allergic Hydroxy Fatty Acids fromFrontiers in pharmacology · 2017
    Article
  7. Review
  8. Short-term physical inactivity impairs vascular function.The Journal of surgical research · 2014
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

5 authors at 1 institution in 1 country.

R J SmithDepartment of Hypersensitivity Diseases Research, Upjohn Co., Kalamazoo, MI 49001.
J M Justen
E G Nidy
L M Sam
J E Bleasdale
W.E. Upjohn Institute for Employment Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

15(S)-Hydroxy-(5Z,8Z,11Z,13E)-eicosatetraenoic acid (15-HETE) exerted a time- and concentration-dependent inhibition of superoxide anion (O2-) production and exocytosis of both azurophil and specific granule constituents from human polymorphonuclear neutrophils (PMN) stimulated with the receptor-specific agonists, N-formylmethionylleucylphenylalanine (FMLP), platelet-activating factor, and leukotriene B4, but not that elicited by phorbol 12-myristate 13-acetate. 15-HETE did not alter the binding of FMLP to its specific receptors on PMN but, rather, appeared to interfere with a subsequent process in signal transduction. Receptor-coupled production of inositol 1,4,5-trisphosphate (InsP3) and increases in cytosolic free calcium elicited with FMLP, platelet-activating factor, and leukotriene B4 were suppressed by 15-HETE. 15-HETE did not, however, inhibit the mobilization of 45Ca from intracellular stores elicited by the addition of InsP3 to permeabilized PMN. 15-HETE suppressed O2- production and increases in intracellular [Ca2+] induced when cell-surface receptors were bypassed and the PMN were activated directly by the guanine nucleotide-binding protein (G protein) activators aluminum fluoride (AlF4-) and mastoparan. 15-HETE, however, did not perturb all G protein functions because cAMP production in FMLP-activated PMN was essentially unaffected by 15-HETE. These data support the proposition that 15-HETE modulates receptor-triggered activation of PMN either by uncoupling G protein stimulation of phospholipase C or by directly inhibiting phospholipase C, thus inhibiting the InsP3-dependent rise in intracellular [Ca2+] that is prerequisite for PMN responsiveness to receptor agonists.

Indexed as

Aluminum CompoundsAluminumCalciumCell DegranulationCell MembraneCyclic AMPFluoridesGTP PhosphohydrolasesGuanosine 5'-O-(3-Thiotriphosphate)HumansHydroxyeicosatetraenoic AcidsInositol 1,4,5-TrisphosphateIntercellular Signaling Peptides and ProteinsIn Vitro TechniquesNeutrophilsN-Formylmethionine Leucyl-Phenylalanine15-hydroxy-5,8,11,13-eicosatetraenoic acidAluminumAluminum Compoundsaluminum fluorideCalciumCyclic AMPFluoridesGTP PhosphohydrolasesGuanosine 5'-O-(3-Thiotriphosphate)Hydroxyeicosatetraenoic AcidsInositol 1,4,5-TrisphosphateIntercellular Signaling Peptides and ProteinsmastoparanN-Formylmethionine Leucyl-PhenylalaninePeptidesProtein Kinase CWasp Venoms

Identifiers

PMID8394015
PMCPMC47118
OpenAlexW2034937689

What OpenQuestion holds

Textmetadata
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.