Evidence map›Paper›PMID 22196923›Full record

ArticleJournal of autoimmunity2012

Anti-phospholipid induced murine fetal loss: novel protective effect of a peptide targeting the β2 glycoprotein I phospholipid-binding site. Implications for human fetal loss.

Yeny Martinez de la Torre, Francesca Pregnolato, Fabio D'Amelio, Claudia Grossi, Nicoletta Di Simone, Fabio Pasqualini, Manuela Nebuloni, Pojen Chen, Silvia Pierangeli, Niccolò Bassani and 5 more

Open access · greenAbstract read
In one paragraph

Article in Journal of autoimmunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
  2. The pathogenesis of obstetric APS: a 2023 update.Clinical immunology (Orlando, Fla.) · 2023
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Emerging Therapies in Antiphospholipid Syndrome.Current rheumatology reports · 2016
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. The autoimmune side of heart and lung diseases.Clinical reviews in allergy & immunology · 2013
    Review
  20. Article
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

15 authors at 6 institutions in 2 countries.

Yeny Martinez de la TorreIstituto Clinico Humanitas, Rozzano, Italy.
Francesca Pregnolato
Fabio D'Amelio
Claudia Grossi
Nicoletta Di Simone
Fabio Pasqualini
Manuela Nebuloni
Pojen Chen
Silvia Pierangeli
Niccolò Bassani
Federico Ambrogi
Maria-Orietta Borghi
Annunciata Vecchi
Massimo Locati
Pier-Luigi Meroni
University of Milan · ITFondazione Humanitas per la Ricerca · ITIRCCS Istituto Auxologico Italiano · ITThe University of Texas Medical Branch at Galveston · USUniversità Cattolica del Sacro Cuore · ITUniversity of California, Los Angeles · US

Funding

Antiphospholipid antibodies and lupus: new molecular targets for treatmentR01AR056745 · NIAMS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI BRASIER, ALLAN R., GONZALEZ, EMILIO B · 2010 to 2014
$1.6M
NIAMS NIH HHS 5R01AR05674502NIAMS NIH HHS R01 AR056745
6 · The paper itself

Abstract

β2 glycoprotein I (β2GPI)-dependent anti-phospholipid antibodies (aPL) induce thrombosis and affect pregnancy. The CMV-derived synthetic peptide TIFI mimics the PL-binding site of β2GPI and inhibits β2GPI cell-binding in vitro and aPL-mediated thrombosis in vivo. Here we investigated the effect of TIFI on aPL-induced fetal loss in mice. TIFI inhibitory effect on in vitro aPL binding to human trophoblasts was evaluated by indirect immunofluorescence and ELISA. TIFI effect on aPL-induced fetal loss was investigated in pregnant C57BL/6 mice treated with aPL or normal IgG (NHS). Placenta/fetus weight and histology and RNA expression were analyzed. TIFI, but not the control peptide VITT, displayed a dose-dependent inhibition of aPL binding to trophoblasts in vitro. Injection of low doses of aPL at day 0 of pregnancy caused growth retardation and increased fetal loss rate, both significantly reduced by TIFI but not VITT. Consistent with observations in humans, histological analysis showed no evidence of inflammation in this model, as confirmed by the absence of an inflammatory signature in gene expression analysis, which in turn revealed a TIFI-dependent modulation of molecules involved in differentiation and development processes. These findings support the non-inflammatory pathogenic role of aPL and suggest innovative therapeutic approaches to aPL-dependent fetal loss.

Indexed as

Abortion, SpontaneousAnimalsAntibodies, Antiphospholipidbeta 2-Glycoprotein IBinding SitesFemaleGene Expression ProfilingHumansMiceMice, Inbred C57BLPeptidesPlacentaPregnancyProtein BindingTrophoblastsAntibodies, Antiphospholipidbeta 2-Glycoprotein IPeptidesTIFI peptide

Identifiers

PMID22196923
PMCPMC3313005
OpenAlexW1975785448

What OpenQuestion holds

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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.