Evidence map›Paper›PMID 19628708›Full record

ArticleBlood2009

Annexin A2 is involved in antiphospholipid antibody-mediated pathogenic effects in vitro and in vivo.

Zurina Romay-Penabad, Maria Guadalupe Montiel-Manzano, Tuya Shilagard, Elizabeth Papalardo, Gracie Vargas, Arun B Deora, Michael Wang, Andrew T Jacovina, Ethel Garcia-Latorre, Elba Reyes-Maldonado and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
9.5field-weighted citation impact, top 1% 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

47 citing papers in PubMed, 133 citations in OpenAlex.

  1. Review
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  6. Pathophysiology of Antiphospholipid Syndrome.Thrombosis and haemostasis · 2022
    Article
  7. Review
  8. Article
  9. Article
  10. Annexin A2 in Fibrinolysis, Inflammation and Fibrosis.International journal of molecular sciences · 2021
    Review
  11. Annexin Animal Models-From Fundamental Principles to Translational Research.International journal of molecular sciences · 2021
    Review
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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

12 authors at 4 institutions in 2 countries.

Zurina Romay-PenabadDivision of Rheumatology, Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX 77555-1165, USA.
Maria Guadalupe Montiel-Manzano
Tuya Shilagard
Elizabeth Papalardo
Gracie Vargas
Arun B Deora
Michael Wang
Andrew T Jacovina
Ethel Garcia-Latorre
Elba Reyes-Maldonado
Katherine A Hajjar
Silvia S Pierangeli
The University of Texas Medical Branch at Galveston · USCornell University · USInstituto Politécnico Nacional · MXMexican Social Security Institute · MX

Funding

YNG1 PHD BINDING TO H3 3METHYL AT K4 PROMOTES TRANSCRIPTION AT TARGETED ORFSP41RR000862 · NCRR · ROCKEFELLER UNIVERSITY · PI DARNELL, JAMES E · 1985 to 2011
$16.1M
NCRR NIH HHS P41 RR000862
6 · The paper itself

Abstract

Antiphospholipid (aPL) antibodies recognize receptor-bound beta(2) glycoprotein I (beta(2)GPI) on target cells, and induce an intracellular signaling and a procoagulant/proinflammatory phenotype that leads to thrombosis. Evidence indicates that annexin A2 (A2), a receptor for tissue plasminogen activator and plasminogen, binds beta(2)GPI on target cells. However, whether A2 mediates pathogenic effects of aPL antibodies in vivo is unknown. In this work, we studied the effects of human aPL antibodies in A2-deficient (A2(-/-)) mice. A2(-/-) and A2(+/+) mice were injected with immunoglobulin G (IgG) isolated from either a patient with antiphospholipid syndrome (IgG-APS), a healthy control subject (IgG-normal human serum), a monoclonal anti-beta(2)GPI antibody (4C5), an anti-A2 monoclonal antibody, or monoclonal antibody of irrelevant specificity as control. We found that, after IgG-APS or 4C5 injections and vascular injury, mean thrombus size was significantly smaller and tissue factor activity was significantly less in A2(-/-) mice compared with A2(+/+) mice. The expression of vascular cell adhesion molecule-1 induced by IgG-APS or 4C5 in explanted A2(-/-) aorta was also significantly reduced compared with A2(+/+) mice. Interestingly, anti-A2 monoclonal antibody significantly decreased aPL-induced expression of intercellular cell adhesion molecule-1, E-selectin, and tissue factor activity on cultured endothelial cells. Together, these data indicate for the first time that A2 mediates the pathogenic effects of aPL antibodies in vivo and in vitro APS.

Indexed as

AnimalsAnnexin A2Antibodies, AntiphospholipidAntiphospholipid SyndromeAortaBlotting, WesternCardiovascular DiseasesCarotid ArteriesCells, CulturedEndothelium, VascularEnzyme-Linked Immunosorbent AssayE-SelectinHumansImmunoglobulin GIntercellular Adhesion Molecule-1In Vitro TechniquesAnnexin A2Antibodies, AntiphospholipidE-SelectinImmunoglobulin GIntercellular Adhesion Molecule-1ThromboplastinVascular Cell Adhesion Molecule-1

Identifiers

PMID19628708
PMCPMC6055708
OpenAlexW2140483523

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.