Evidence map›Paper›PMID 11701087›Full record

ArticleBMC cell biology2001

Deciphering the plasma membrane hallmarks of apoptotic cells: phosphatidylserine transverse redistribution and calcium entry.

M C Martínez, J M Freyssinet

Open access · goldAbstract read
In one paragraph

Article in BMC cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

22 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Phosphatidylserine-positive extracellular vesicles boost effector CD8Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Review
  4. Article
  5. The Role of Exosomes in Cancer Progression.International journal of molecular sciences · 2021
    Review
  6. Extracellular Vesicles in Skin Wound Healing.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  7. Review
  8. Review
  9. Review
  10. Journal of extracellular vesicles · 2020
    Article
  11. Review
  12. Review
  13. TTB2 induces apoptosis in Ewing sarcoma cells.Experimental and therapeutic medicine · 2018
    Article
  14. Phospholipid subcellular localization and dynamics.The Journal of biological chemistry · 2018
    Review
  15. Exosomes: new molecular targets of diseases.Acta pharmacologica Sinica · 2018
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Exclusion of ABCA-1 as a candidate gene for canine Scott syndrome.Journal of thrombosis and haemostasis : JTH · 2008
    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

2 authors at 2 institutions in 1 country.

M C MartínezInstitut d'Hématologie et d'Immunologie, Faculté de Médecine, Université Louis Pasteur, 4, rue Kirschleger, 67085, Strasbourg, France. carmen.martinez@hemato-ulp.u-strasbg.fr
J M Freyssinet
Inserm · FRInstitut de Virologie · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDuring apoptosis, Ca2+-dependent events participate in the regulation of intracellular and morphological changes including phosphatidylserine exposure in the exoplasmic leaflet of the cell plasma membrane. The occurrence of phosphatidylserine at the surface of specialized cells, such as platelets, is also essential for the assembly of the enzyme complexes of the blood coagulation cascade, as demonstrated by hemorrhages in Scott syndrome, an extremely rare genetic deficiency of phosphatidylserine externalization, without other apparent pathophysiologic consequences. We have recently reported a reduced capacitative Ca2+ entry in Scott cells which may be part of the Scott phenotype.

resultsTaking advantage of these mutant lymphoblastoid B cells, we have studied the relationship between this mode of Ca2+ entry and phosphatidylserine redistribution during apoptosis. Ca2+ ionophore induced apoptosis in Scott but not in control cells. However, inhibition of store-operated Ca2+ channels led to caspase-independent DNA fragmentation and decrease of mitochondrial membrane potential in both control and Scott cells. Inhibition of cytochrome P450 also reduced capacitative Ca2+ entry and induced apoptosis at comparable extents in control and Scott cells. During the apoptotic process, both control and more markedly Scott cells externalized phosphatidylserine, but in the latter, this membrane feature was however dissociated from several other intracellular changes.

conclusionsThe present results suggest that different mechanisms account for phosphatidylserine transmembrane migration in cells undergoing stimulation and programmed death. These observations testify to the plasticity of the plasma membrane remodeling process, allowing normal apoptosis even when less fundamental functions are defective.

Indexed as

ApoptosisBiological TransportCalcimycinCalciumCalcium Channel BlockersCalcium ChannelsCell LineCell MembraneCytochrome P-450 Enzyme InhibitorsDNA FragmentationEnzyme InhibitorsHumansImidazolesIonophoresMembrane PotentialsMitochondria1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazoleCalcimycinCalciumCalcium Channel BlockersCalcium ChannelsCytochrome P-450 Enzyme InhibitorsEnzyme InhibitorsImidazolesIonophoresPhosphatidylserinesProadifen

Identifiers

PMID11701087
PMCPMC59679
OpenAlexW2160975723

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.