Evidence map›Paper›PMID 20675368›Full record

ArticleThe Journal of biological chemistry2010

Tilapia hepcidin 2-3 peptide modulates lipopolysaccharide-induced cytokines and inhibits tumor necrosis factor-alpha through cyclooxygenase-2 and phosphodiesterase 4D.

Venugopal Rajanbabu, Chieh-Yu Pan, Shang-Chun Lee, Wei-Ju Lin, Ching-Chun Lin, Chung-Leung Li, Jyh-Yih Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Immune Modulation Ability of Hepcidin from Teleost Fish.Animals : an open access journal from MDPI · 2022
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Antimicrobial peptides from fish.Pharmaceuticals (Basel, Switzerland) · 2014
    Article
  12. Article
  13. Article
  14. Article
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 3 institutions in 1 country.

Venugopal RajanbabuMarine Research Station, Institute of Cellular and Organismic Biology, Academia Sinica, 262 Jiaushi, Taiwan.
Chieh-Yu Pan
Shang-Chun Lee
Wei-Ju Lin
Ching-Chun Lin
Chung-Leung Li
Jyh-Yih Chen
Institute of Cellular and Organismic Biology, Academia Sinica · TWGenomics Research Center, Academia Sinica · TWNational Chung Hsing University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The antimicrobial peptide, tilapia hepcidin (TH) 2-3, belongs to the hepcidin family, and its antibacterial function has been reported. Here, we examined the TH2-3-mediated regulation of proinflammatory cytokines in bacterial endotoxin lipopolysaccharide (LPS)-stimulated mouse macrophages. The presence of TH2-3 in LPS-stimulated cells reduced the amount of tumor necrosis factor (TNF)-α secretion. From a microarray, real-time polymerase chain reaction (PCR), and cytokine array studies, we showed down-regulation of the proinflammatory cytokines TNF-α, interleukin (IL)-1α, IL-1β, IL-6, and the prostaglandin synthesis gene, cyclooxygenase (COX)-2, by TH2-3. Studies with the COX-2-specific inhibitor, melaxicam, and with COX-2-overexpressing cells demonstrated the positive regulation of TNF-α and negative regulation of cAMP degradation-specific phosphodiesterase (PDE) 4D by COX-2. In LPS-stimulated cells, TH2-3 acts like melaxicam and down-regulates COX-2 and up-regulates PDE4D. The reduction in intracellular cAMP by TH2-3 or melaxicam in LPS-stimulated cells supports the negative regulation of PDE4D by COX-2 and TH2-3. This demonstrates that the inhibition of COX-2 is among the mechanisms through which TH2-3 controls TNF-α release. At 1 h after treatment, the presence of TH2-3 in LPS-stimulated cells had suppressed the induction of pERK1/2 and prevented the LPS-stimulated nuclear accumulation of NF-κB family proteins of p65, NF-κB2, and c-Rel. In conclusion, TH2-3 inhibits TNF-α and other proinflammatory cytokines through COX-2-, PDE4D-, and pERK1/2-dependent mechanisms.

Indexed as

TilapiaAnimalsAntimicrobial Cationic PeptidesCell LineCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 4Cyclooxygenase 2Fish ProteinsHepcidinsInterleukin-1alphaInterleukin-1betaInterleukin-6LipopolysaccharidesMacrophagesMiceMitogen-Activated Protein Kinase 3Antimicrobial Cationic PeptidesCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 4Cyclooxygenase 2Fish ProteinsHamp protein, mouseHepcidinsInterleukin-1alphaInterleukin-1betaInterleukin-6lipopolysaccharide, Escherichia coli O111 B4LipopolysaccharidesMitogen-Activated Protein Kinase 3NF-kappa B p52 SubunitPDE4D protein, mousePtgs2 protein, mouseRela protein, mouseTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID20675368
PMCPMC2945552
OpenAlexW2087766484

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.