Evidence map›Paper›PMID 9763444›Full record

ArticleMolecular biology of the cell1998

Fibroblast growth factor (FGF) soluble receptor 1 acts as a natural inhibitor of FGF2 neurotrophic activity during retinal degeneration.

X Guillonneau, F Régnier-Ricard, O Laplace, L Jonet, M Bryckaert, Y Courtois, F Mascarelli

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
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  7. All Good Things Must End: Termination of Receptor Tyrosine Kinase Signal.International journal of molecular sciences · 2021
    Review
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  12. Design of growth factor sequestering biomaterials.Chemical communications (Cambridge, England) · 2014
    Review
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  15. Characterization of the basic fibroblast growth factor-evoked proliferation of the human Müller cell line, MIO-M1.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2004
    Article
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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

7 authors at 2 institutions in 1 country.

X GuillonneauDéveloppement, Vieillissement et Pathologie de la Rétine, Institut National de la Santé et de la Recherche Médicale U450, Affiliée Centre National de la Recherche Scientifique, Association Claude Bernard, 75016 Paris, France.
F Régnier-Ricard
O Laplace
L Jonet
M Bryckaert
Y Courtois
F Mascarelli
Université Claude Bernard Lyon 1 · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factors (FGF) 1 and 2 and their tyrosine kinase receptor (FGFR) are present throughout the adult retina. FGFs are potential mitogens, but adult retinal cells are maintained in a nonproliferative state unless the retina is damaged. Our work aims to find a modulator of FGF signaling in normal and pathological retina. We identified and sequenced a truncated FGFR1 form from rat retina generated by the use of selective polyadenylation sites. This 70-kDa form of soluble extracellular FGFR1 (SR1) was distributed mainly localized in the inner nuclear layer of the retina, whereas the full-length FGFR1 form was detected in the retinal Muller glial cells. FGF2 and FGFR1 mRNA levels greatly increased in light-induced retinal degeneration. FGFR1 was detected in the radial fibers of activated retinal Muller glial cells. In contrast, SR1 mRNA synthesis followed a biphasic pattern of down- and up-regulation, and anti-SR1 staining was intense in retinal pigmented epithelial cells. The synthesis of SR1 and FGFR1 specifically and independently regulated in normal and degenerating retina suggests that changes in the proportion of various FGFR forms may control the bioavailability of FGFs and thus their potential as neurotrophic factors. This was demonstrated in vivo during retinal degeneration when recombinant SR1 inhibited the neurotrophic activity of exogenous FGF2 and increased damaging effects of light by inhibiting endogenous FGF. This study highlights the significance of the generation of SR1 in normal and pathological conditions.

Indexed as

Transcription, GeneticAmino Acid SequenceAnimalsBase SequenceCells, CulturedErbB ReceptorsExonsFibroblast Growth Factor 1Fibroblast Growth Factor 2Gene Expression RegulationHumansLightMiceMolecular Sequence DataPigment Epithelium of EyeRatsErbB ReceptorsFibroblast Growth Factor 1Fibroblast Growth Factor 2Receptor Protein-Tyrosine KinasesReceptors, Fibroblast Growth FactorRNA, Messenger

Identifiers

PMID9763444
PMCPMC25554
OpenAlexW2161716890

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.