Evidence map›Paper›PMID 12709026›Full record

ArticleImmunology2003

TRAF6-NF-kappaB pathway is essential for interleukin-1-induced TLR2 expression and its functional response to TLR2 ligand in murine hepatocytes.

Takayuki Matsumura, Takahiro Degawa, Takemasa Takii, Hidetoshi Hayashi, Takashi Okamoto, Jun-ichiro Inoue, Kikuo Onozaki

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Gut-liver axis at the frontier of host-microbial interactions.American journal of physiology. Gastrointestinal and liver physiology · 2017
    Review
  10. Immune Dysfunction in Cirrhosis.Journal of clinical and translational hepatology · 2017
    Review
  11. AFrontiers in cellular and infection microbiology · 2017
    Article
  12. Review
  13. Hypoxia-inducible factor-2α induces expression of type X collagen and matrix metalloproteinases 13 in osteoarthritic meniscal cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    Article
  14. Article
  15. Article
  16. Article
  17. Hepatic TLR4 signaling in obese NAFLD.American journal of physiology. Gastrointestinal and liver physiology · 2015
    Article
  18. Review
  19. Review
  20. 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

7 authors at 2 institutions in 1 country.

Takayuki MatsumuraDepartment of Molecular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, Japan.
Takahiro Degawa
Takemasa Takii
Hidetoshi Hayashi
Takashi Okamoto
Jun-ichiro Inoue
Kikuo Onozaki
Nagoya City University · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously reported that the expressions of TLR2 and TLR4 mRNA are differentially regulated in mouse liver and in the parenchymal cells. In the present study, we investigated the mechanism of the up-regulatory effects of interleukin-1alpha (IL-1alpha), tumour necrosis factor-alpha (TNF-alpha), lipopolysaccharide (LPS), or bacterial lipoprotein (BLP) on TLR2 mRNA expression in primary cultured murine hepatocytes. Although TLR2 mRNA stability was not affected, these treatments enhanced NF-kappaB activity and TLR2 gene transcription simultaneously. The up-regulation of TLR2 transcription in response to these reagents was completely inhibited by blocking the NF-kappaB activation pathway, demonstrating a pivotal role of NF-kappaB activation in the regulation of hepatocyte TLR2 transcription. The expression of TLR2 protein by hepatocytes was also remarkably up-regulated by IL-1alpha and, to a lesser extent, by TNF-alpha as well, but not by LPS or BLP. In addition, pretreatment of mice with IL-1alpha markedly increased the BLP (a ligand for TLR2)-induced serum level of serum amyloid A (SAA), an acute-phase protein predominantly produced by hepatocytes, indicating that IL-1alpha may also up-regulate functional TLR2 in vivo. These results demonstrate that IL-1alpha, through activating the TRAF6-NF-kappaB pathway, serves as the most potent inducer for TLR2 up-regulation, and plays an important role in the regulation of hepatocyte functions by augmenting the hepatocyte response to bacteria or bacterial products.

Indexed as

AnimalsBacterial ProteinsCells, CulturedFemaleHepatocytesInterleukin-1LigandsLipopolysaccharidesMembrane GlycoproteinsMiceMice, Inbred ICRNF-kappa BProteinsReceptors, Cell SurfaceRNA, MessengerSerum Amyloid A ProteinBacterial ProteinsInterleukin-1LigandsLipopolysaccharidesMembrane GlycoproteinsNF-kappa BProteinsReceptors, Cell SurfaceRNA, MessengerSerum Amyloid A ProteinTNF Receptor-Associated Factor 6Toll-Like Receptor 2Toll-Like Receptor 4Toll-Like ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID12709026
PMCPMC1782941
OpenAlexW2010156274

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.