Evidence map›Paper›PMID 23760670›Full record

ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2013

Ranibizumab efficiently blocks migration but not proliferation induced by growth factor combinations including VEGF in retinal endothelial cells.

Heidrun L Deissler, Helmut Deissler, Gerhard K Lang, Gabriele E Lang

Abstract read
In one paragraph

Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Article
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  5. Article
  6. Article
  7. Binding of VEGF-A is sufficient to abrogate the disturbing effects of VEGF-B together with VEGF-A on retinal endothelial cells.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2015
    Article
  8. 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

4 authors.

Heidrun L DeisslerDepartment of Ophthalmology, University of Ulm, Prittwitzstrasse 43, 89075, Ulm, Germany, heidrun.deissler@uniklinik-ulm.de.
Helmut Deissler
Gerhard K Lang
Gabriele E Lang

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProliferation and migration of retinal endothelial cells (REC) are associated with the development of proliferative diabetic retinopathy. REC proliferation is stimulated by isoforms of vascular endothelial growth factor-A (i.e., VEGF₁₂₁ and VEGF₁₆₅), basic fibroblast growth factor (bFGF), and insulin-like growth factor (IGF-1) of which VEGF₁₆₅ also enhances migration of REC. Effects induced by VEGF-A can be blocked with ranibizumab, a VEGF-binding Fab fragment used in therapy of diabetic macular edema. In this study, we investigated potential angiogenic effects of placental growth factors (PlGF-1, PlGF-2) as other members of the VEGF family and whether the primary action of VEGF₁₆₅ is modulated in the presence of bFGF, IGF-1 and PlGF-1/-2. We also studied how effects of growth factor combinations can be attenuated with ranibizumab.

methodsEffects of single growth factors or their combinations on proliferation and migration of immortalized bovine retinal endothelial cells (iBREC) were studied with or without ranibizumab or the inhibitor of VEGF receptors KRN951.

resultsProliferation of iBREC was significantly stimulated by 1-100 ng/ml PlGF-1 or PlGF-2, but additive effects were not observed with various combinations of the tested growth factors. Ranibizumab neutralized VEGF's effect on proliferation but was not effective when the other growth factors were used in combination with VEGF. bFGF and IGF-1 but not PlGF-1 or PlGF-2 stimulated iBREC migration as single agents, and they further enhanced VEGF-induced migration. The effects of such growth factor combinations including VEGF on migration were efficiently blocked by targeting only VEGF with ranibizumab. Migration induced by VEGF plus bFGF and IGF-1 was also almost completely inhibited by KRN951 interfering with VEGF receptor signalling.

conclusionsMigration but not proliferation of iBREC induced by combinations of bFGF, IGF-1, PlGF-1 or PlGF-2 together with VEGF is efficiently suppressed by ranibizumab. VEGF-mediated signalling through VEGFR2 seems to control REC migration dominantly in the presence of other growth factors.

Indexed as

Angiogenesis InhibitorsAnimalsAntibodies, Monoclonal, HumanizedCattleCell LineCell MovementCell ProliferationDrug CombinationsEndothelial CellsFibroblast Growth Factor 2Insulin-Like Growth Factor IIntercellular Signaling Peptides and ProteinsPhenylurea CompoundsPlacenta Growth FactorPregnancy ProteinsQuinolinesAngiogenesis InhibitorsAntibodies, Monoclonal, HumanizedDrug CombinationsFibroblast Growth Factor 2Insulin-Like Growth Factor IIntercellular Signaling Peptides and ProteinsPhenylurea CompoundsPlacenta Growth FactorPregnancy ProteinsQuinolinesRanibizumabReceptors, Vascular Endothelial Growth FactortivozanibVascular Endothelial Growth Factor A

Identifiers

PMID23760670
PMCPMC3777160

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Registered trials

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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.