Evidence map›Paper›PMID 19809821›Full record

ArticleRheumatology international2010

Regulation of TNFalpha and IL1beta in rheumatoid arthritis synovial fibroblasts by leukotriene B4.

Shaohua Xu, Houshan Lu, Jianhao Lin, Zhankun Chen, Dongfang Jiang

Abstract read
PubMed Publisher
In one paragraph

Article in Rheumatology international, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Lipid metabolism and rheumatoid arthritis.Frontiers in immunology · 2023
    Review
  4. Lipidomic Profiling in Synovial Tissue.Frontiers in medicine · 2022
    Review
  5. Lipid Metabolism Profiles in Rheumatic Diseases.Frontiers in pharmacology · 2021
    Review
  6. Article
  7. In vivo amelioration of endogenous antitumor autoantibodies via low-dose P4N through the LTA4H/activin A/BAFF pathway.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  8. Review
  9. Persisting eicosanoid pathways in rheumatic diseases.Nature reviews. Rheumatology · 2014
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. 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

5 authors at 1 institution in 1 country.

Shaohua XuArthritis Institute, Peking University, Beijing, China.
Houshan Lu
Jianhao Lin
Zhankun Chen
Dongfang Jiang
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arachidonic acid metabolites, such as leukotriene B4 (LTB4), are known to play an important role in pathogenesis of rheumatoid arthritis (RA). Apart from leukocytes, RA synovial fibroblasts (RASF) produce a broad array of inflammatory mediators to recruit, retain and activate immune cells and resident mesenchymal cells in the joints to promote ongoing inflammation and tissue destruction. To determine how LTB4 may contribute to this process, RASF was cultured from synovial tissues collected from RA patients undergoing total knee replacement. The level of LTB4 in culture medium was determined using ELISA, and expression of LTB4 receptors (BLT1 and BLT2) by RT-PCR. In the presence of exogenous LTB4, mRNA and protein levels of tumor necrosis factor-alpha (TNFalpha) and interleukin 1beta (IL1beta) were determined by real-time PCR and ELISA. Furthermore, we examined the effects of leukotrienes synthesis inhibitors, MK886 and bestatin, on mRNA and protein levels of TNFalpha and IL1beta in RASF. We found that LTB4 was present at a low concentration in the culture medium of RASF, and the major LTB4 receptor expressed in RASF was BLT2. LTB4 synthesis was activated by treatment with LIT (LPS, ionomycin and thapsogargin), and suppressed by MK886 and bestatin. Exogenous LTB4 remarkably increased the expression of TNFalpha and IL1beta at both the mRNA level and the protein level. In contrast, MK886 and bestatin significantly inhibited their expression. These data suggested that LTB4 contributed to RA by regulating the expression of TNFalpha and IL1beta in RASF. BLT2 was probably the major receptor mediating such effects.

Indexed as

Arthritis, RheumatoidFibroblastsHumansInflammation MediatorsInterleukin-1betaLeukocytesLeukotriene B4LipopolysaccharidesReceptors, Leukotriene B4Reverse Transcriptase Polymerase Chain ReactionRNA, MessengerSynovial MembraneTumor Necrosis Factor-alphaInflammation MediatorsInterleukin-1betaLeukotriene B4LipopolysaccharidesLTB4R protein, humanReceptors, Leukotriene B4RNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID19809821
OpenAlexW2047965244

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.