Evidence map›Paper›PMID 29847841›Full record

ArticleThrombosis and haemostasis2018

Vascular Permeability and Remodelling Coincide with Inflammatory and Reparative Processes after Joint Bleeding in Factor VIII-Deficient Mice.

Esther J Cooke, Jenny Y Zhou, Tine Wyseure, Shweta Joshi, Vikas Bhat, Donald L Durden, Laurent O Mosnier, Annette von Drygalski

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Thrombosis and haemostasis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.4field-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

31 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  16. Article
  17. Hemophilic arthropathy: Current knowledge and future perspectives.Journal of thrombosis and haemostasis : JTH · 2021
    Review
  18. Article
  19. Article
  20. Haemophilia.Nature reviews. Disease primers · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Esther J CookeDivision of Hematology/Oncology, Department of Medicine, University of California San Diego, La Jolla, California, United States.
Jenny Y ZhouDivision of Hematology/Oncology, Department of Medicine, University of California San Diego, La Jolla, California, United States.
Tine WyseureDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California, United States.
Shweta JoshiDepartment of Pediatrics, Moores UCSD Cancer Center, University of California San Diego, La Jolla, California, United States.
Vikas BhatDivision of Hematology/Oncology, Department of Medicine, University of California San Diego, La Jolla, California, United States.
Donald L DurdenDepartment of Pediatrics, Moores UCSD Cancer Center, University of California San Diego, La Jolla, California, United States.
Laurent O MosnierDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California, United States.
Annette von DrygalskiDivision of Hematology/Oncology, Department of Medicine, University of California San Diego, La Jolla, California, United States.
Scripps Research Institute · USUniversity of California, San Diego · US

Funding

Structure-function of cytoprotective coagulation proteases and their receptorsR01HL104165 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI MOSNIER, LAURENT OLIVIER · 2011 to 2024
$6.1M
Discovery of novel vascular therapies targeting PfEMP1-mediated cytoadhesion in severe malariaR01HL130678 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI LAVSTSEN, THOMAS, MOSNIER, LAURENT OLIVIER · 2015 to 2018
$2.0M
Development of the first-in-class novel dual PI-3K/BRD4 inhibitor SF2523R42CA192656 · NCI · SIGNALRX PHARMACEUTICALS, INC. · PI MORALES, GUILLERMO A · 2017 to 2018
$2.0M
Role of PTEN and PI-3 Kinase in MedulloblastomagenesisR01CA172513 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DURDEN, DONALD · 2017 to 2023
$1.6M
Maximal MYC control using dual PI-3K/BRD4 (kinase/epigenetic) inhibitorsR41CA192656 · NCI · SIGNALRX PHARMACEUTICALS, INC. · PI DURDEN, DONALD · 2015 to 2015
$209k
NCI NIH HHS R01 CA172513NCI NIH HHS R41 CA192656NCI NIH HHS R42 CA192656NHLBI NIH HHS R01 HL104165NHLBI NIH HHS R01 HL130678
6 · The paper itself

Abstract

Vascular remodelling is a prominent feature of haemophilic arthropathy (HA) that may underlie re-bleeding, yet the nature of vascular changes and underlying mechanisms remain largely unknown. Here, we aimed to characterize synovial vascular remodelling and vessel integrity after haemarthrosis, as well as temporal changes in inflammatory and tissue-reparative pathways. Thirty acutely painful joints in patients with haemophilia (PWH) were imaged by musculoskeletal ultrasound with Power Doppler (MSKUS/PD) to detect vascular abnormalities and bloody effusions. Nineteen out of 30 painful joint episodes in PWH were associated with haemarthrosis, and abnormal vascular perfusion was unique to bleeding joints. A model of induced haemarthrosis in factor VIII (FVIII)-deficient mice was used for histological assessment of vascular remodelling (α-smooth muscle actin [αSMA] expression), and monitoring of in vivo vascular perfusion and permeability by MSKUS/PD and albumin extravasation, respectively. Inflammatory (M1) and reparative (M2) macrophage markers were quantified in murine synovium over a 10-week time course by real-time polymerase chain reaction. The abnormal vascular perfusion observed in PWH was recapitulated in FVIII-deficient mice after induced haemarthrosis. Neovascularization and increased vessel permeability were apparent 2 weeks post-bleed in FVIII-deficient mice, after a transient elevation of inflammatory macrophage M1 markers. These vascular changes subsided by week 4, while vascular remodelling, evidenced by architectural changes and pronounced αSMA expression, persisted alongside a reparative macrophage M2 response. In conclusion, haemarthrosis leads to transient inflammation coupled with neovascularization and associated vascular permeability, while subsequent tissue repair mechanisms coincide with vascular remodelling. Together, these vascular changes may promote re-bleeding and HA progression.

Indexed as

ActinsAdultAnimalsCapillary PermeabilityDisease Models, AnimalFactor VIIIFemaleHemarthrosisHemophilia AHumansInflammationKnee JointMacrophagesMaleMiceMice, Inbred BALB CActa2 protein, mouseActinsFactor VIII

Identifiers

PMID29847841
PMCPMC6191040
OpenAlexW2805057092

What OpenQuestion holds

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Registered trials

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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.