Evidence map›Paper›PMID 21990354›Full record

ArticleThe Journal of biological chemistry2011

Inflammatory macrophages induce Nrf2 transcription factor-dependent proteasome activity in colonic NCM460 cells and thereby confer anti-apoptotic protection.

Susanne Sebens, Iris Bauer, Claudia Geismann, Evelin Grage-Griebenow, Stefan Ehlers, Marie-Luise Kruse, Alexander Arlt, Heiner Schäfer

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 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 4 institutions in 1 country.

Susanne SebensDepartment of Internal Medicine I, Laboratory of Molecular Gastroenterology & Hepatology, Universitätsklinikum Schleswig Holstein-Campus Kiel, Kiel, Germany.
Iris Bauer
Claudia Geismann
Evelin Grage-Griebenow
Stefan Ehlers
Marie-Luise Kruse
Alexander Arlt
Heiner Schäfer
University Hospital Schleswig-Holstein · DEUniversitäts Hautklinik Kiel · DEUniversity of Lübeck · DEResearch Center Borstel - Leibniz Lung Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adaptation of epithelial cells to persistent oxidative stress plays an important role in inflammation-associated carcinogenesis. This adaptation process involves activation of Nrf2 (nuclear factor-E2-related factor-2), which has been recently shown to contribute to carcinogenesis through the induction of proteasomal gene expression and proteasome activity. To verify this possible link between inflammation, oxidative stress, and Nrf2-dependent proteasome activation, we explored the impact of inflammatory (M1) macrophages on the human colon epithelial cell line NCM460. Transwell cocultures with macrophages differentiated from granulocyte monocyte-colony-stimulating factor-treated monocytes led to an increased activity of Nrf2 in NCM460 cells along with an elevated proteasome activity. This higher proteasome activity resulted from Nrf2-dependent induction of proteasomal gene expression, as shown for the 19 and 20 S subunit proteins S5a and α5, respectively. These effects of macrophage coculture were preceded by an increase of reactive oxygen species in cocultured NCM460 cells and could be blocked by catalase or by the reactive oxygen species scavenger Tiron, whereas transient treatment of NCM460 cells with H(2)O(2) similarly led to Nrf2-dependent proteasome activation. Through the Nrf2-dependent increase of proteasomal gene expression and proteasome activity, the sensitivity of NCM460 cells to tumor necrosis factor-related apoptosis-inducing ligand- or irinotecan-induced apoptosis declined. These findings indicate that inflammatory conditions such as the presence of M1 macrophages and the resulting oxidative stress are involved in the Nrf2-dependent gain of proteasome activity in epithelial cells, e.g. colonocytes, giving rise of greater resistance to apoptosis. This mechanism might contribute to inflammation-associated carcinogenesis, e.g. of the colon.

Indexed as

ApoptosisCamptothecinCell LineCoculture TechniquesColonGene Expression Regulation, EnzymologicHumansInflammationIntracellular SpaceIrinotecanMacrophagesNF-E2-Related Factor 2Proteasome Endopeptidase ComplexReactive Oxygen SpeciesTNF-Related Apoptosis-Inducing LigandCamptothecinIrinotecanNF-E2-Related Factor 2Proteasome Endopeptidase ComplexReactive Oxygen SpeciesTNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID21990354
PMCPMC3220482
OpenAlexW2071027952

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.