Evidence map›Paper›PMID 15743796›Full record

ArticleThe American journal of pathology2005

A cyclosporine-sensitive psoriasis-like disease produced in Tie2 transgenic mice.

Daniel Voskas, Nina Jones, Paul Van Slyke, Celina Sturk, Wing Chang, Alex Haninec, Yael Olya Babichev, Jennifer Tran, Zubin Master, Stephen Chen and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. 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
4.7field-weighted citation impact, top 4% 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, 90 citations in OpenAlex.

  1. Review
  2. Polymorphisms inArchives of endocrinology and metabolism · 2023
    Article
  3. Adaptor Protein ShcD/Molecular cancer research : MCR · 2021
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Psoriasis: what we have learned from mouse models.Nature reviews. Rheumatology · 2010
    Review
  15. Evidence for altered Wnt signaling in psoriatic skin.The Journal of investigative dermatology · 2010
    Article
  16. Article
  17. Angiogenesis drives psoriasis pathogenesis.International journal of experimental pathology · 2009
    Review
  18. Article
  19. 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

19 authors at 5 institutions in 2 countries.

Daniel VoskasDepartment of Medical Biophysics, University of Toronto, Toronto, Canada.
Nina Jones
Paul Van Slyke
Celina Sturk
Wing Chang
Alex Haninec
Yael Olya Babichev
Jennifer Tran
Zubin Master
Stephen Chen
Nicole Ward
Maribelle Cruz
Jamie Jones
Robert S Kerbel
Serge Jothy
Lina Dagnino
Jack Arbiser
Giannoula Klement
Daniel J Dumont
Sunnybrook Health Science Centre · CAWestern University · CACase Western Reserve University · USEmory University · USSt. Michael's Hospital · CA

Funding

Genetic Control of Vascular RemodelingR01HL063224 · NHLBI · SUNNYBROOK &WOMEN'S COLL HLTH SCIS CTR · PI DUMONT, DANIEL J · 2001 to 2004
$824k
NHLBI NIH HHS HL63224-01NHLBI NIH HHS R01 HL063224
6 · The paper itself

Abstract

Psoriasis is a common, persistent skin disorder characterized by recurrent erythematous lesions thought to arise as a result of inflammatory cell infiltration and activation of keratinocyte proliferation. Unscheduled angiogenic growth has also been proposed to mediate the pathogenesis of psoriasis although the cellular and molecular basis for this response remains unclear. Recently, a role for the angiopoietin signaling system in psoriasis has been suggested by studies that demonstrate an up-regulation of the tyrosine kinase receptor Tie2 (also known as Tek) as well as angiopoietin-1 and angiopoietin-2 in human psoriatic lesions. To examine temporal expression of Tie2, we have developed a binary transgenic approach whereby expression of Tie2 can be conditionally regulated by the presence of tetracycline analogs in double-transgenic mice. A psoriasis-like phenotype developed in double-transgenic animals within 5 days of birth and persisted throughout adulthood. The skin of affected mice exhibited many cardinal features of human psoriasis including epidermal hyperplasia, inflammatory cell accumulation, and altered dermal angiogenesis. These skin abnormalities resolved completely with tetracycline-mediated suppression of transgene expression, thereby illustrating a complete dependence on Tie2 signaling for disease maintenance and progression. Furthermore, the skin lesions in double-transgenic mice markedly improved after administration of the immunosuppressive anti-psoriatic agent cyclosporine, thus demonstrating the clinical significance of this new model.

Indexed as

AngiopoietinsAnimalsBlotting, WesternCell LineCyclosporineDoxycyclineEnzyme-Linked Immunosorbent AssayEpidermisGene Expression RegulationGenotypeHumansImmunohistochemistryImmunoprecipitationImmunosuppressive AgentsInflammationKeratinocytesAngiopoietinsCyclosporineDoxycyclineImmunosuppressive AgentsLectinsReceptor, TIE-2TetracyclineVascular Endothelial Growth Factor A

Identifiers

PMID15743796
PMCPMC1602355
OpenAlexW2020845827

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.