Evidence map›Paper›PMID 18450586›Full record

ArticleInvestigative ophthalmology & visual science2008

Vascular endothelial growth factor induces MEF2C and MEF2-dependent activity in endothelial cells.

Debasish Maiti, Zhenhua Xu, Elia J Duh

Abstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  13. The "Angiogenic Switch" and Functional Resources in Cyclic Sports Athletes.International journal of molecular sciences · 2021
    Review
  14. Molecular Features of Cancer-associated Fibroblast Subtypes and their Implication on Cancer Pathogenesis, Prognosis, and Immunotherapy Resistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    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

3 authors at 1 institution in 1 country.

Debasish MaitiDepartment of Ophthalmology, Wilmer Ophthalmological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA.
Zhenhua Xu
Elia J Duh
Johns Hopkins University · US

Funding

Role and regulation of MEF2C in retinal angiogenesisR01EY018138 · NEI · JOHNS HOPKINS UNIVERSITY · PI DUH, ELIA J · 2007 to 2011
$1.8M
GENE EXPRESSION CHANGES IN RETINAL NEOVASCULARIZATIONK08EY000398 · NEI · JOHNS HOPKINS UNIVERSITY · PI DUH, ELIA J · 1999 to 2003
$703k
NEI NIH HHS EY00398NEI NIH HHS EY018138NEI NIH HHS K08 EY000398NEI NIH HHS R01 EY018138
6 · The paper itself

Abstract

purposeVascular endothelial growth factor is a key regulator of physiological and pathologic angiogenesis. Although much is known about the major upstream signaling pathways of VEGF in endothelial cells, less is known about key transcription factors involved in VEGF action. The transcription factor myocyte enhancer factor (MEF)-2C is thought to play an important role in vasculogenesis and angiogenesis during vascular development. The purpose of this study was to investigate the regulation of MEF2C expression and MEF2-dependent activity in endothelial cells by VEGF.

methodsExpression of MEF2C in human retinal endothelial cells and human umbilical vein endothelial cells was assayed by real-time PCR and Western blot. VEGF regulation of MEF2-dependent transcription was studied using an MEF2-luciferase reporter construct containing three copies of a high-affinity MEF2 binding site. The effect of MEF2 on endothelial cell migration was evaluated using a dominant-negative MEF2C mutant.

resultsVEGF induced MEF2C expression in a dose- and time-dependent fashion. This induction was completely abrogated by the inhibition of protein kinase C and was partially blocked by the inhibition of PKC-beta and PKC-delta. In addition to regulating MEF2C expression, VEGF stimulated transcription from an MEF2-dependent promoter. VEGF stimulation of transcription was significantly reduced by the inhibition of calcineurin, CaMKII, p38 MAPK, and PKC, but not by the inhibition of ERK1/2 or BMK1/ERK5. Transfection of a dominant-negative mutant of MEF2C significantly inhibited VEGF-stimulated endothelial cell migration.

conclusionsThese results implicate VEGF as a key regulator of MEF2C and suggest that MEF2 may be an important mediator of VEGF in endothelial cells.

Indexed as

Blotting, WesternCell Culture TechniquesCell MovementDose-Response Relationship, DrugEndothelium, VascularGene Expression RegulationHumansMADS Domain ProteinsMEF2 Transcription FactorsMyogenic Regulatory FactorsPlasmidsProtein Kinase CRecombinant ProteinsRetinal VesselsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerMADS Domain ProteinsMEF2C protein, humanMEF2 Transcription FactorsMyogenic Regulatory FactorsProtein Kinase CRecombinant ProteinsRNA, MessengerVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID18450586
PMCPMC4519038
OpenAlexW2002744059

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.