Evidence map›Paper›PMID 28663253›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2017

Inner Mitochondrial Membrane Disruption Links Apoptotic and Agonist-Initiated Phosphatidylserine Externalization in Platelets.

Hyo-Jung Choo, Andaleb Kholmukhamedov, ChengZing Zhou, Shawn Jobe

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Preanalytical conditions for multiparameter platelet flow cytometry.Research and practice in thrombosis and haemostasis · 2023
    Article
  6. Review
  7. Article
  8. Frontiers in pharmacology · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. COVID-19 patients exhibit reduced procoagulant platelet responses.Journal of thrombosis and haemostasis : JTH · 2020
    Article
  13. Article
  14. Article
  15. Review
  16. Procoagulant Phosphatidylserine-Exposing PlateletsFrontiers in cardiovascular medicine · 2020
    Review
  17. Article
  18. Review
  19. Parkin the bus to manage stress.EMBO molecular medicine · 2019
    Article
  20. CD36 signaling in vascular redox stress.Free radical biology & medicine · 2019
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Hyo-Jung ChooFrom the BloodCenter of Wisconsin, Milwaukee (A.K., S.J.); Emory University School of Medicine, Department of Pediatrics and Children's Healthcare of Atlanta, GA (H.-J.C., C.Z., S.J.); Emory University, School of Medicine, Department of Cell Biology, Atlanta, GA (H.-J.C.); and Medical College of Wisconsin, Department of Pediatrics, Milwaukee (S.J.).
Andaleb KholmukhamedovFrom the BloodCenter of Wisconsin, Milwaukee (A.K., S.J.); Emory University School of Medicine, Department of Pediatrics and Children's Healthcare of Atlanta, GA (H.-J.C., C.Z., S.J.); Emory University, School of Medicine, Department of Cell Biology, Atlanta, GA (H.-J.C.); and Medical College of Wisconsin, Department of Pediatrics, Milwaukee (S.J.).
ChengZing ZhouFrom the BloodCenter of Wisconsin, Milwaukee (A.K., S.J.); Emory University School of Medicine, Department of Pediatrics and Children's Healthcare of Atlanta, GA (H.-J.C., C.Z., S.J.); Emory University, School of Medicine, Department of Cell Biology, Atlanta, GA (H.-J.C.); and Medical College of Wisconsin, Department of Pediatrics, Milwaukee (S.J.).
Shawn JobeFrom the BloodCenter of Wisconsin, Milwaukee (A.K., S.J.); Emory University School of Medicine, Department of Pediatrics and Children's Healthcare of Atlanta, GA (H.-J.C., C.Z., S.J.); Emory University, School of Medicine, Department of Cell Biology, Atlanta, GA (H.-J.C.); and Medical College of Wisconsin, Department of Pediatrics, Milwaukee (S.J.). shawn.jobe@bcw.edu.
Versiti Blood Center of Wisconsin · USEmory University · US

Funding

Atlanta Clinical and Translational Science Institute (ACTSI) RenewalUL1TR000454 · NCATS · EMORY UNIVERSITY · PI STEPHENS, DAVID S · 2012 to 2016
$25.8M
The platelet mitochondrial permeability transition and thrombosisR01HL095858 · NHLBI · VERSITI WISCONSIN, INC. · PI JOBE, SHAWN M. · 2009 to 2013
$1.9M
FEI Transmission Electron Microscope with Tomography CapabilityS10RR025679 · NCRR · EMORY UNIVERSITY · PI SPEARMAN, PAUL W. · 2009 to 2009
$500k
NCATS NIH HHS UL1 TR000454NCRR NIH HHS S10 RR025679NHLBI NIH HHS R01 HL095858
6 · The paper itself

Abstract

objectivePhosphatidylserine exposure mediates platelet procoagulant function and regulates platelet life span. Apoptotic, necrotic, and integrin-mediated mechanisms have been implicated as intracellular determinants of platelet phosphatidylserine exposure. Here, we investigate (1) the role of mitochondrial events in platelet phosphatidylserine exposure initiated by these distinct stimuli and (2) the cellular interactions of the procoagulant platelet in vitro and in vivo. APPROACH AND

resultsKey mitochondrial events were examined, including cytochrome c release and inner mitochondrial membrane (IMM) disruption. In both ABT-737 (apoptotic) and agonist (necrotic)-treated platelets, phosphatidylserine externalization was temporally correlated with IMM disruption. Agonist stimulation resulted in rapid cyclophilin D-dependent IMM disruption that coincided with phosphatidylserine exposure. ABT-737 treatment caused rapid cytochrome c release, eventually followed by caspase-dependent IMM disruption that again closely coincided with phosphatidylserine exposure. A nonmitochondrial and integrin-mediated mechanism has been implicated in the formation of a novel phosphatidylserine-externalizing platelet subpopulation. Using image cytometry, this subpopulation is demonstrated to be the result of the interaction of an aggregatory platelet and a procoagulant platelet rather than indicative of a novel intracellular mechanism regulating platelet phosphatidylserine externalization. Using electron microscopy, similar interactions between aggregatory and procoagulant platelets are demonstrated in vitro and in vivo within a mesenteric vein hemostatic thrombus.

conclusionsPlatelet phosphatidylserine externalization is closely associated with the mitochondrial event of IMM disruption identifying a common pathway in phosphatidylserine-externalizing platelets. The limited interaction of procoagulant platelets and integrin-active aggregatory platelets identifies a potential mechanism for procoagulant platelet retention within the hemostatic thrombus.

Indexed as

ApoptosisPlatelet AggregationAnimalsbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinBiphenyl CompoundsBlood CoagulationBlood PlateletsCaspasesCrotalid VenomsCyclophilinsCytochromes cDisease Models, AnimalGenotypeIntegrinsKineticsABT-737Bak1 protein, mouseBax protein, mousebcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinBiphenyl CompoundsCaspasesconvulxinCrotalid VenomsCyclophilinsCytochromes cIntegrinsLectins, C-TypeNitrophenolsPeptidyl-Prolyl Isomerase FPhosphatidylserinesPiperazinesPPIF protein, mouseSulfonamidesThrombinblood plateletcell deathcytosolmitochondrial membranephosphatidylserine

Identifiers

PMID28663253
PMCPMC5560492
OpenAlexW2731863865

What OpenQuestion holds

Textmetadata
LicenceTDM
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.