Evidence map›Paper›PMID 18058124›Full record

ArticlePflugers Archiv : European journal of physiology2008

Inhibition of suicidal erythrocyte death by nitric oxide.

Jan P Nicolay, Gerd Liebig, Olivier M Niemoeller, Saisudha Koka, Mehrdad Ghashghaeinia, Thomas Wieder, Judith Haendeler, Rudi Busse, Florian Lang

Abstract read
PubMed Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Apoptosis and eryptosis: similarities and differences.Apoptosis : an international journal on programmed cell death · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Ion Transport in Eryptosis, the Suicidal Death of Erythrocytes.Frontiers in cell and developmental biology · 2020
    Review
  13. Article
  14. Article
  15. Manipulating Eryptosis of Human Red Blood Cells: A Novel Antimalarial Strategy?Frontiers in cellular and infection microbiology · 2018
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  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

9 authors at 3 institutions in 1 country.

Jan P NicolayDepartment of Physiology, University of Tübingen, Tübingen, Germany.
Gerd Liebig
Olivier M Niemoeller
Saisudha Koka
Mehrdad Ghashghaeinia
Thomas Wieder
Judith Haendeler
Rudi Busse
Florian Lang
University of Tübingen · DEGoethe University Frankfurt · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nitric oxide (NO) is known to counteract apoptosis by S-nitrosylation of protein thiol groups. NO is generated and stored in erythrocytes, which may undergo eryptosis, a suicidal cell death similar to apoptosis of nucleated cells. Eryptosis is triggered by increased cytosolic Ca2+ activity and/or ceramide and characterized by cell shrinkage and phosphatidylserine exposure at the cell surface. The present study explored whether nitric oxide could interfere with the machinery underlying eryptosis. To this end, erythrocyte phosphatidylserine exposure (annexin V-binding) and cell volume (forward scatter) were determined by flow cytometry. The Ca2+ ionophore ionomycin (0.1 microM) increased cytosolic Ca2+ activity, triggered annexin binding, and decreased forward scatter. The annexin binding and decrease of forward scatter but not the increase of cytosolic Ca2+ activity were reversed by the NO-donor nitroprusside (1 microM) and papanonoate (100 microM). Higher concentrations of nitroprusside (0.1 and 1 mM) stimulated eryptosis. Glucose depletion, exposure to C6-ceramide (3 microM), hypertonic (addition of 550 mM sucrose), and isotonic (replacement of Cl- with gluconate) cell shrinkage all triggered annexin V binding, effects all reversed by nitroprusside (1 microM). Dibutyryl-cGMP (1 mM) blunted the ionomycin- but not the ceramide-induced annexin V binding. Ionomycin decreased protein nitrosylation and thioredoxin activity, effects reversed by the NO-donor papanonoate. Clearance of erythrocytes from circulating blood was significantly faster in eNOS knockout mice than in their wild-type littermates. In conclusion, nitric oxide participates in the regulation of erythrocyte survival, an effect partially mimicked by cGMP and paralleled by alterations of protein nitrosylation and thioredoxin activity.

Indexed as

AnimalsAnnexinsApoptosisCalciumCeramidesCyclic GMPErythrocyte MembraneErythrocytesFluoresceinsFluorescent DyesHumansIonomycinIonophoresMiceMice, KnockoutNitric Oxide5-(6)-carboxyfluorescein diacetate succinimidyl esterAnnexinsCalciumCeramidesCyclic GMPFluoresceinsFluorescent DyesIonomycinIonophoresN-(alpha-hydroxyoctadecanoyl)phytosphingosineNitric OxideNitroprussidePhosphatidylserinesSuccinimides

Identifiers

PMID18058124
OpenAlexW2165745548

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.