Evidence map›Paper›PMID 22517312›Full record

ArticleMolecular medicine (Cambridge, Mass.)2012

Sprouty is a negative regulator of transforming growth factor β-induced epithelial-to-mesenchymal transition and cataract.

Eun Hye H Shin, M Albert Basson, Michael L Robinson, John W McAvoy, Frank J Lovicu

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2012. 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
2.1field-weighted citation impact, top 13% 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, 50 citations in OpenAlex.

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  14. The murine lens: A model to investigate in vivo epithelial-mesenchymal transition.Developmental dynamics : an official publication of the American Association of Anatomists · 2018
    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

5 authors at 4 institutions in 3 countries.

Eun Hye H ShinAnatomy and Histology, Bosch Institute & Save Sight Institute, University of Sydney, Sydney, Australia.
M Albert Basson
Michael L Robinson
John W McAvoy
Frank J Lovicu
University of Sydney · AUKing's College London · GBMiami University · USRobert Bosch (Australia) · AU

Funding

STUDIES ON LENS DIFFERENTIATION: ROLE OF FGFR01EY003177 · NEI · UNIVERSITY OF SYDNEY · PI LOVICU, FRANK JAMES, MCAVOY, JOHNSTON W · 1985 to 2015
$1.8M
Medical Research Council G0601104NEI NIH HHS R01 EY003177NEI NIH HHS R01 EY03177
6 · The paper itself

Abstract

Fibrosis affects an extensive range of organs and is increasingly acknowledged as a major component of many chronic disorders. It is now well accepted that the elevated expression of certain inflammatory cell-derived cytokines, especially transforming growth factor β (TGFβ), is involved in the epithelial-to-mesenchymal transition (EMT) leading to the pathogenesis of a diverse range of fibrotic diseases. In lens, aberrant TGFβ signaling has been shown to induce EMT leading to cataract formation. Sproutys (Sprys) are negative feedback regulators of receptor tyrosine kinase (RTK)-signaling pathways in many vertebrate systems, and in this study we showed that they are important in the murine lens for promoting the lens epithelial cell phenotype. Conditional deletion of Spry1 and Spry2 specifically from the lens leads to an aberrant increase in RTK-mediated extracellular signal-regulated kinase 1/2 phosphorylation and, surprisingly, elevated TGFβ-related signaling in lens epithelial cells, leading to an EMT and subsequent cataract formation. Conversely, increased Spry overexpression in lens cells can suppress not only TGFβ-induced signaling, but also the accompanying EMT and cataract formation. On the basis of these findings, we propose that a better understanding of the relationship between Spry and TGFβ signaling will not only elucidate the etiology of lens pathology, but will also lead to the development of treatments for other fibrotic-related diseases associated with TGFβ-induced EMT.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCataractEpithelial CellsEpithelial-Mesenchymal TransitionIntracellular Signaling Peptides and ProteinsLens, CrystallineMembrane ProteinsMiceMice, KnockoutPhosphoproteinsProtein Serine-Threonine KinasesSignal TransductionTransforming Growth Factor betaAdaptor Proteins, Signal TransducingIntracellular Signaling Peptides and ProteinsMembrane ProteinsPhosphoproteinsProtein Serine-Threonine KinasesSpry1 protein, mouseSpry2 protein, mouseTransforming Growth Factor beta

Identifiers

PMID22517312
PMCPMC3409273
OpenAlexW56524497

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.