Evidence map›Paper›PMID 19011018›Full record

ArticleInvestigative ophthalmology & visual science2009

CTGF is increased in basal deposits and regulates matrix production through the ERK (p42/p44mapk) MAPK and the p38 MAPK signaling pathways.

Norihiro Nagai, Alena Klimava, Wen-Hsiang Lee, Kanako Izumi-Nagai, James T Handa

Open access · greenAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

33 citing papers in PubMed, 52 citations in OpenAlex.

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  16. CTGF Contributes to the Development of Posterior Capsule Opacification: anInternational journal of biological sciences · 2018
    Article
  17. Minireview: Fibronectin in retinal disease.Experimental biology and medicine (Maywood, N.J.) · 2017
    Review
  18. 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

5 authors at 1 institution in 1 country.

Norihiro NagaiWilmer Eye Institute, Johns Hopkins School of Medicine, Baltimore, Maryland 21287, USA.
Alena Klimava
Wen-Hsiang Lee
Kanako Izumi-Nagai
James T Handa
Johns Hopkins Medicine · US

Funding

AGE-induced Phenotype of the Retinal Pigment EpitheliumR01EY014005 · NEI · JOHNS HOPKINS UNIVERSITY · PI HANDA, JAMES T · 2001 to 2015
$6.4M
NEI NIH HHS EY14005NEI NIH HHS R01 EY014005
6 · The paper itself

Abstract

purposeMatrix expansion is an early change in age-related maculopathy. The aim of this study was to determine whether connective tissue growth factor (CTGF) regulates the production of extracellular matrix components by retinal pigmented epithelial (RPE) cells.

methodsARPE-19 cells were treated with CTGF and analyzed for fibronectin, laminin, and MMP-2 by RT-qPCR, Western blot analysis, or zymography. Cells were also pretreated with an MEK-1/2 inhibitor (PD98059) or a p38 inhibitor (SB203580) and an anti-CTGF antibody to analyze the signaling contributing to fibronectin, laminin, and MMP-2 production. Human maculas were analyzed for mRNA using laser capture microdissected RPE cells and by immunohistochemistry for the topographic distribution of CTGF.

resultsCTGF induced fibronectin mRNA (P=0.006) and protein (P=0.006), and laminin mRNA (P=0.006) and protein (P=0.02) by ARPE-19 cells. CTGF also induced MMP-2 mRNA (P=0.002) and protein secretion (P=0.04). Using zymography, CTGF increased the latent and active forms of MMP-2 compared to controls (P=0.02). An anti-CTGF antibody inhibited fibronectin, laminin, and MMP-2 after CTGF stimulation. CTGF increased the phosphorylation of p38 and ERK1/2. Fibronectin and MMP-2 mRNA and protein were suppressed by a MEK-1/2 inhibitor, but not with a p38 inhibitor. Laminin expression was suppressed by both inhibitors. RT-qPCR analysis showed that macular RPE cells from human donors express CTGF. Immunohistochemistry of human maculas showed strong labeling of CTGF in Bruch membrane, including basal deposits and drusen.

conclusionsCTGF is increased in basal deposits and drusen of AMD specimens, and it induces matrix protein production in ARPE-19 cells through the ERK (p42/p44(mapk)) and p38(mapk) signaling pathways.

Indexed as

Basement MembraneBlotting, WesternCells, CulturedConnective Tissue Growth FactorExtracellular Matrix ProteinsFibronectinsFlavonoidsHumansImidazolesImmunoenzyme TechniquesLamininMatrix Metalloproteinase 2Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3p38 Mitogen-Activated Protein KinasesPyridines2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneCCN2 protein, humanConnective Tissue Growth FactorExtracellular Matrix ProteinsFibronectinsFlavonoidsImidazolesLamininMatrix Metalloproteinase 2Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3p38 Mitogen-Activated Protein KinasesPyridinesRecombinant ProteinsRNA, MessengerSB 203580

Identifiers

PMID19011018
PMCPMC2729056
OpenAlexW1996353160

What OpenQuestion holds

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LicenceTDM
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.