Evidence map›Paper›PMID 38820498›Full record

ArticleBlood2024

4D intravital imaging studies identify platelets as the predominant cellular procoagulant surface in a mouse hemostasis model.

Abigail Ballard-Kordeliski, Robert H Lee, Ellen C O'Shaughnessy, Paul Y Kim, Summer R Jones, Rafal Pawlinski, Matthew J Flick, David S Paul, Nigel Mackman, David A Adalsteinsson and 1 more

Abstract read
In one paragraph

Article in Blood, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Review
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  4. Plg-RMolecular medicine (Cambridge, Mass.) · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Abigail Ballard-KordeliskiDepartment of Biochemistry and Biophysics, The University of North Carolina at Chapel Hill, Chapel Hill, NC.ORCID 0000-0002-7773-1093
Robert H LeeDepartment of Biochemistry and Biophysics, The University of North Carolina at Chapel Hill, Chapel Hill, NC.ORCID 0000-0001-9871-0593
Ellen C O'ShaughnessyDepartment of Cell Biology and Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC.
Paul Y KimDepartment of Medicine, McMaster University, Hamilton, ON, Canada.ORCID 0000-0002-0504-3064
Summer R JonesDepartment of Biochemistry and Biophysics, The University of North Carolina at Chapel Hill, Chapel Hill, NC.
Rafal PawlinskiUNC Blood Research Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC.ORCID 0000-0001-5162-7135
Matthew J FlickUNC Blood Research Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC.
David S PaulDepartment of Biochemistry and Biophysics, The University of North Carolina at Chapel Hill, Chapel Hill, NC.
Nigel MackmanUNC Blood Research Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC.ORCID 0000-0002-9170-7700
David A AdalsteinssonDepartment of Mathematics, The University of North Carolina at Chapel Hill, Chapel Hill, NC.
Wolfgang BergmeierDepartment of Biochemistry and Biophysics, The University of North Carolina at Chapel Hill, Chapel Hill, NC.ORCID 0000-0002-1211-8861

Funding

The Hemostasis, Thrombosis, and Inflammation Models CoreP01HL151433 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Wolfgang Bergmeier · 2020 to 2026
$16.4M
Tissue factor-dependent coagulation in thrombosis and immune responsesR35HL155657 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Nigel Mackman · 2021 to 2026
$5.5M
Small GTPases in the biology of platelets and megakaryocytesR35HL144976 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BERGMEIER, WOLFGANG · 2019 to 2025
$5.4M
Reprogramming PDAC Stroma by Targeting Coagulation in the Tumor MicroenvironmentU01CA274304 · NCI · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI Melissa L. Fishel, Matthew J. Flick · 2022 to 2026
$4.6M
Mechanism of sickle cell disease-specific venous thromboembolismR01HL157441 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KEY, NIGEL S., PAWLINSKI, RAFAL L · 2021 to 2024
$2.6M
Mechanisms linking the plasminogen/fibrinogen axis to the pathogenesis of COVID-19R01HL160046 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FLICK, MATTHEW J., GRALINSKI, LISA · 2021 to 2024
$2.2M
Novel mechanisms to limit thrombosis by decreasing fibrinogen or suppressing fibrin matrix formationR01HL168009 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Matthew J. Flick, Christian Kastrup · 2024 to 2026
$2.2M
The Role of the small GTPase Rap1 in Platelet-Coagulation InterplayF31HL165935 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BALLARD, ABIGAIL RENE · 2022 to 2024
$118k
NCI NIH HHS U01 CA274304NHLBI NIH HHS F31 HL165935NHLBI NIH HHS P01 HL151433NHLBI NIH HHS R01 HL157441NHLBI NIH HHS R01 HL160046NHLBI NIH HHS R01 HL168009NHLBI NIH HHS R35 HL144976NHLBI NIH HHS R35 HL155657
6 · The paper itself

Abstract

abstractInterplay between platelets, coagulation factors, endothelial cells (ECs), and fibrinolytic factors is necessary for effective hemostatic plug formation. This study describes a 4-dimensional (4D) imaging platform to visualize and quantify hemostatic plug components in mice with high spatiotemporal resolution. Fibrin accumulation after laser-induced vascular injury was observed at the platelet plug-EC interface, controlled by the antagonistic balance between fibrin generation and breakdown. We observed less fibrin accumulation in mice expressing low levels of tissue factor or F12-/-mice compared with controls, whereas increased fibrin accumulation, including on the vasculature adjacent to the platelet plug, was observed in plasminogen-deficient mice or wild-type mice treated with tranexamic acid. Phosphatidylserine (PS), a membrane lipid critical for the assembly of coagulation factors, was first detected at the platelet plug-EC interface, followed by exposure across the endothelium. Impaired PS exposure resulted in a significant reduction in fibrin accumulation in cyclophilin D-/-mice. Adoptive transfer studies demonstrated a key role for PS exposure on platelets, and to a lesser degree on ECs, in fibrin accumulation during hemostatic plug formation. Together, these studies suggest that (1) platelets are the functionally dominant procoagulant cellular surface, and (2) plasmin is critical for limiting fibrin accumulation at the site of a forming hemostatic plug.

Indexed as

Blood PlateletsFibrinHemostasisAnimalsBlood CoagulationDisease Models, AnimalEndothelial CellsIntravital MicroscopyMiceMice, Inbred C57BLMice, KnockoutPhosphatidylserinesThromboplastinFibrinPhosphatidylserinesThromboplastin

Identifiers

PMID38820498
PMCPMC11406176

What Socratic 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 Socratic graph.