Evidence map›Paper›PMID 21303922›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2011

Regulation of transforming growth factor-β1-dependent integrin β6 expression by p38 mitogen-activated protein kinase in bile duct epithelial cells.

Bradley P Sullivan, Karen M Kassel, Sharon Manley, Alyson K Baker, James P Luyendyk

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Integrin Alpha v Beta 6 (αvβ6) and Its Implications in Cancer Treatment.International journal of molecular sciences · 2022
    Review
  3. Modulation of αExperimental & molecular medicine · 2021
    Article
  4. Review
  5. Article
  6. ETS2 promotes epithelial-to-mesenchymal transition in renal fibrosis by targeting JUNB transcription.Laboratory investigation; a journal of technical methods and pathology · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Autocrine regulation of biliary pathology by activated cholangiocytes.American journal of physiology. Gastrointestinal and liver physiology · 2012
    Review
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.

Bradley P SullivanDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, 3901 Rainbow Blvd, MS-1018, Kansas City, KS 66160, USA.
Karen M Kassel
Sharon Manley
Alyson K Baker
James P Luyendyk
University of Kansas Medical Center · US

Funding

THE ROLE OF HUMAN PXR IN ANTI-TUBERCULOSIS DRUG-INDUCED LIVER INJURYP20RR021940 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI KLASSEN, CURTIS D · 2006 to 2011
$12.1M
TRAINING PROGRAM IN ENVIRONMENTAL TOXICOLOGYT32ES007079 · NIEHS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI HAGENBUCH, BRUNO · 1985 to 2015
$4.1M
Novel anti-fibrotic mechanisms in chemical-induced liver injuryR01ES017537 · NIEHS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LUYENDYK, JAMES P · 2009 to 2019
$3.6M
NCRR NIH HHS P20 RR021940NIEHS NIH HHS R01 ES017537NIEHS NIH HHS R01-ES017537NIEHS NIH HHS T32 ES007079NIEHS NIH HHS T32ES007079
6 · The paper itself

Abstract

Bile duct epithelial cells (BDECs) contribute to liver fibrosis by expressing αVβ6 integrin, a critical activator of latent transforming growth factor β (TGF-β). β6 integrin (Itgβ6) mRNA induction and αVβ6 integrin expression in BDECs are partially TGF-β-dependent. However, the signaling pathways required for TGF-β-dependent Itgβ6 mRNA induction in BDECs are not known. We tested the hypothesis that the p38 mitogen-activated protein kinase (MAPK) signaling pathway contributes to TGF-β1 induction of Itgβ6 mRNA by activating SMAD and activator protein 1 (AP-1) transcription factors. Pretreatment of transformed human BDECs (MMNK-1 cells) with two different p38 MAPK inhibitors, but not a control compound, inhibited TGF-β1 induction of Itgβ6 mRNA. Inhibition of p38 also reduced TGF-β1 activation of a SMAD-dependent reporter construct. Expression of a dominant-negative SMAD3 (SMAD3ΔC) significantly reduced TGF-β1-induced Itgβ6 mRNA expression. Expression of JunB mRNA, but not other AP-1 proteins, increased in TGF-β1-treated MMNK-1 cells, and induction of JunB expression was p38-dependent. Consistent with a requirement for de novo induction of JunB protein, cycloheximide pretreatment inhibited TGF-β1 induction of Itgβ6 mRNA. Expression of a dominant-negative AP-1 mutant (TAM67) also inhibited TGF-β1 induction of Itgβ6 mRNA. Overall, the results suggest that p38 contributes to TGF-β1-induced Itgβ6 mRNA expression in MMNK-1 cells by regulating activation of both SMAD and AP-1 transcription factors.

Indexed as

Bile DuctsBlotting, WesternCell LineCytosolDensitometryDNA, ComplementaryEpithelial CellsHumansImmunoprecipitationIntegrin beta ChainsLuciferasesp38 Mitogen-Activated Protein KinasesReverse Transcriptase Polymerase Chain ReactionRNARNA, Small InterferingSignal TransductionDNA, Complementaryintegrin beta6Integrin beta ChainsLuciferasesp38 Mitogen-Activated Protein KinasesRNARNA, Small InterferingSmad3 ProteinTranscription Factor AP-1Transforming Growth Factor beta1

Identifiers

PMID21303922
PMCPMC3083106
OpenAlexW2156756264

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.