Evidence map›Paper›PMID 17407446›Full record

ArticleThe Biochemical journal2007

Activation of NADPH oxidase by transforming growth factor-beta in hepatocytes mediates up-regulation of epidermal growth factor receptor ligands through a nuclear factor-kappaB-dependent mechanism.

Miguel M Murillo, Irene Carmona-Cuenca, Gaelle Del Castillo, Conrad Ortiz, César Roncero, Aránzazu Sánchez, Margarita Fernández, Isabel Fabregat

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 101 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Miguel M MurilloFundació Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), Centre d'Oncologia Molecular, L'Hospitalet, Barcelona, Spain.
Irene Carmona-Cuenca
Gaelle Del Castillo
Conrad Ortiz
César Roncero
Aránzazu Sánchez
Margarita Fernández
Isabel Fabregat
Universidad Complutense de Madrid · ESInstitut d'Investigació Biomédica de Bellvitge · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The TGF-beta (transforming growth factor-beta) induces survival signals in foetal rat hepatocytes through transactivation of EGFR (epidermal growth factor receptor). The molecular mechanism is not completely understood, but both activation of the TACE (tumour necrosis factor alpha-converting enzyme)/ADAM17 (a disintegrin and metalloproteinase 17; one of the metalloproteases involved in shedding of the EGFR ligands) and up-regulation of TGF-alpha and HB-EGF (heparin-binding epidermal growth factor-like growth factor) appear to be involved. In the present study, we have analysed the molecular mechanisms that mediate up-regulation of the EGFR ligands by TGF-beta in foetal rat hepatocytes. The potential involvement of ROS (reactive oxygen species), an early signal induced by TGF-beta, and the existence of an amplification loop triggered by initial activation of the EGFR, have been studied. Results indicate that DPI (diphenyleneiodonium) and apocynin, two NOX (NADPH oxidase) inhibitors, and SB431542, an inhibitor of the TbetaR-I (TGF-beta receptor I), block up-regulation of EGFR ligands and Akt activation. Different members of the NOX family of genes are expressed in hepatocytes, included nox1, nox2 and nox4. TGF-beta up-regulates nox4 and increases the levels of Rac1 protein, a known regulator of both Nox1 and Nox2, in a TbetaR-I-dependent manner. TGF-beta mediates activation of the nuclear factor-kappaB pathway, which is inhibited by DPI and is required for up-regulation of TGF-alpha and HB-EGF. In contrast, EGFR activation is not required for TGF-beta-induced up-regulation of those ligands. Considering previous work that has established the role of ROS in apoptosis induced by TGF-beta in hepatocytes, the results of the present study indicate that ROS might mediate both pro- and anti-apoptotic signals in TGF-beta-treated cells.

Indexed as

AcetophenonesAnimalsAnthracenesBenzamidesChromonesDioxolesEnzyme ActivationEpidermal Growth FactorErbB ReceptorsExtracellular Signal-Regulated MAP KinasesFlavonoidsHeparin-binding EGF-like Growth FactorHepatocytesHumansImidazolesIntercellular Signaling Peptides and Proteins2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one2-(4-nitrophenyl)-4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazole4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamideAcetophenonesacetovanilloneAnthracenesBenzamidesChromonesDioxolesdiphenyleneiodoniumEpidermal Growth FactorErbB ReceptorsExtracellular Signal-Regulated MAP KinasesFlavonoidsHBEGF protein, humanHbegf protein, ratHeparin-binding EGF-like Growth FactorImidazolesIntercellular Signaling Peptides and ProteinsMorpholinesNADH, NADPH OxidoreductasesNADPH Oxidase 1NADPH Oxidase 4NADPH OxidasesNF-kappa BNOX1 protein, ratNox4 protein, ratOnium CompoundsPeptidesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktpyrazolanthroneQuinazolinesrac1 GTP-Binding ProteinRac1 protein, ratReactive Oxygen SpeciesRTKI cpdSN50 peptideTransforming Growth Factor betaTyrphostins

Identifiers

PMID17407446
PMCPMC1904531
OpenAlexW2103868295

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.