Evidence map›Paper›PMID 21700930›Full record

ArticleCirculation research2011

AIP1 prevents graft arteriosclerosis by inhibiting interferon-γ-dependent smooth muscle cell proliferation and intimal expansion.

Luyang Yu, Lingfeng Qin, Haifeng Zhang, Yun He, Hong Chen, Jordan S Pober, George Tellides, Wang Min

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.5field-weighted citation impact, top 18% 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, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Cellular signaling pathways of T cells in giant cell arteritis.Journal of geriatric cardiology : JGC · 2021
    Article
  8. Review
  9. Article
  10. Fibroblast-specific Stat1 deletion enhances the myofibroblast phenotype during tissue repair.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. Recent advances in allograft vasculopathy.Current opinion in organ transplantation · 2017
    Review
  15. Review
  16. Article
  17. Article
  18. A Novel Monoclonal Antibody Against Human DAB2IP.Monoclonal antibodies in immunodiagnosis and immunotherapy · 2015
    Article
  19. Article
  20. Review
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

8 authors at 2 institutions in 1 country.

Luyang YuInterdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.
Lingfeng Qin
Haifeng Zhang
Yun He
Hong Chen
Jordan S Pober
George Tellides
Wang Min
China Medical University · CNAffiliated Hospital of Liaoning University of Traditional Chinese Medicine · CN

Funding

SOCS-1 and endothelial dysfunction in graft arteriosclerosisP01HL070295 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2001 to 2010
$17.9M
INHIBITING JNK, A NEW ANTI-INFLAMMATORY STRATEGYR01HL065978 · NHLBI · YALE UNIVERSITY · PI MIN, WANG · 2000 to 2010
$3.9M
STRESS SIGNALING PATHWAYS LINKING ENDOTHELIAL INJURY TO GRAFT ARTERIOSCLEROSISR01HL109420 · NHLBI · YALE UNIVERSITY · PI POBER, JORDAN S · 2012 to 2020
$3.3M
Thioredoxin and Endothelial Cell FunctionR01HL085789 · NHLBI · YALE UNIVERSITY · PI MIN, WANG · 2008 to 2012
$2.1M
TNF receptor-2 signaling in arteriogenesis/angiogenesisR01HL077357 · NHLBI · YALE UNIVERSITY · PI MIN, WANG · 2007 to 2010
$1.7M
NHLBI NIH HHS P01 HL070295NHLBI NIH HHS P01HL070295NHLBI NIH HHS R01 HL065978NHLBI NIH HHS R01 HL077357NHLBI NIH HHS R01 HL085789NHLBI NIH HHS R01 HL109420
6 · The paper itself

Abstract

rationaleASK1-interacting protein-1 (AIP1), a Ras GTPase-activating protein family member, is highly expressed in endothelial cells and vascular smooth musccells (VSMCs). The role of AIP1 in VSMCs and VSMC proliferative disease is not known.

objectiveWe used mouse graft arteriosclerosis models characterized by VSMC accumulation and intimal expansion to determine the function of AIP1. METHODS AND

resultsIn a single minor histocompatibility antigen (male to female)-dependent aorta transplantation model, AIP1 deletion in the graft augmented neointima formation, an effect reversed in AIP1/interferon-γ receptor (IFN-γR) doubly-deficient aorta donors. In a syngeneic aortic transplantation model in which wild-type or AIP1-knockout mouse aortas were transplanted into IFN-γR-deficient recipients and in which neointima formation was induced by intravenous administration of an adenovirus that encoded a mouse IFN-γ transgene, donor grafts from AIP1-knockout mice enhanced IFN-γ-induced VSMC proliferation and neointima formation. Mechanistically, knockout or knockdown of AIP1 in VSMCs significantly enhanced IFN-γ-induced JAK-STAT signaling and IFN-γ-dependent VSMC migration and proliferation, 2 critical steps in neointima formation. Furthermore, AIP1 specifically bound to JAK2 and inhibited its activity.

conclusionsAIP1 functions as a negative regulator in IFN-γ-induced intimal formation, in part by downregulating IFN-γ-JAK2-STAT1/3-dependent migratory and proliferative signaling in VSMCs.

Indexed as

Cell ProliferationAnimalsAorta, AbdominalAorta, ThoracicArteriosclerosisCell MovementCells, CulturedDisease Models, AnimalHumansInterferon-gammaInterferon gamma ReceptorJanus Kinase 2MaleMiceMice, KnockoutMinor Histocompatibility AntigensDab2ip protein, mouseInterferon-gammaInterferon gamma ReceptorJak2 protein, mouseJanus Kinase 2Minor Histocompatibility Antigensras GTPase-Activating ProteinsReceptors, InterferonStat1 protein, mouseSTAT1 Transcription FactorStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID21700930
PMCPMC3227522
OpenAlexW2159204615

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.