Evidence map›Paper›PMID 2116419›Full record

ArticleThe Journal of cell biology1990

Role of the membrane skeleton in preventing the shedding of procoagulant-rich microvesicles from the platelet plasma membrane.

J E Fox, C D Austin, J K Boyles, P K Steffen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 157 citations in OpenAlex.

  1. Article
  2. Article
  3. The Progress of Platelets in Breast Cancer.Cancer management and research · 2023
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Actin Cytoskeletal Dynamics in Single-Cell Wound Repair.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. The biology of extracellular vesicles with focus on platelet microparticles and their role in cancer development and progression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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

4 authors at 2 institutions in 1 country.

J E FoxGladstone Foundation Laboratories for Cardiovascular Disease, Department of Pathology, University of California, San Francisco 94140-0608.
C D Austin
J K Boyles
P K Steffen
Gladstone Institutes · USUniversity of California, San Francisco · US

Funding

CONTRACTILE PROTEINS AND PLATELET FUNCTIONR37HL030657 · NHLBI · CLEVELAND CLINIC LERNER COL/MED-CWRU · PI FOX, JOAN E.B. · 1995 to 2004
$2.5M
THE ROLE OF CONTRACTILE PROTEINS IN PLATELET FUNCTIONR01HL030657 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI FOX, JOAN E.B. · 1986 to 1994
–
THE ROLE OF CONTRACTILE PROTEINS IN PLATELET FUNCTIONR23HL030657 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI FOX, JOAN E.B. · 1985 to 1985
–
NHLBI NIH HHS HL-30657
6 · The paper itself

Abstract

The platelet plasma membrane is lined by a membrane skeleton that appears to contain short actin filaments cross-linked by actin-binding protein. Actin-binding protein is in turn associated with specific plasma membrane glycoproteins. The aim of this study was to determine whether the membrane skeleton regulates properties of the plasma membrane. Platelets were incubated with agents that disrupted the association of the membrane skeleton with membrane glycoproteins. The consequences of this change on plasma membrane properties were examined. The agents that were used were ionophore A23187 and dibucaine. Both agents activated calpain (the Ca2(+)-dependent protease), resulting in the hydrolysis of actin-binding protein and decreased association of actin with membrane glycoproteins. Disruption of actin-membrane interactions was accompanied by the shedding of procoagulant-rich microvesicles from the plasma membrane. The shedding of microvesicles correlated with the hydrolysis of actin-binding protein and the disruption of actin-membrane interactions. When the calpain-induced disruption of actin-membrane interactions was inhibited, the shedding of microvesicles was inhibited. These data are consistent with the hypothesis that association of the membrane skeleton with the plasma membrane maintains the integrity of the plasma membrane, preventing the shedding of procoagulant-rich microvesicles from the membrane of unstimulated platelets. They raise the possibility that the procoagulant-rich microvesicles that are released under a variety of physiological and pathological conditions may result from the dissociation of the platelet membrane skeleton from its membrane attachment sites.

Indexed as

ActinsAdultBlood Coagulation FactorsBlood PlateletsCalcimycinCalpainCarrier ProteinsCell FractionationCell MembraneDibucaineElectrophoresis, Polyacrylamide GelHumansKineticsMicroscopy, ElectronMolecular WeightPlatelet Membrane GlycoproteinsActinsBlood Coagulation FactorsCalcimycinCalpainCarrier ProteinsDibucainePlatelet Membrane Glycoproteinsplatelet procoagulant factor

Identifiers

PMID2116419
PMCPMC2116218
OpenAlexW2114530818

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.