Evidence map›Paper›PMID 16014680›Full record

ArticleAnnals of the rheumatic diseases2005

Inhibition of c-kit tyrosine kinase by imatinib mesylate induces apoptosis in mast cells in rheumatoid synovia: a potential approach to the treatment of arthritis.

A Juurikivi, C Sandler, K A Lindstedt, P T Kovanen, T Juutilainen, M J Leskinen, T Mäki, K K Eklund

Open access · bronzeAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

40 citing papers in PubMed, 105 citations in OpenAlex.

  1. Trial
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  9. Optimizing drug inhibition of IgE-mediated anaphylaxis in mice.The Journal of allergy and clinical immunology · 2022
    Article
  10. Article
  11. Review
  12. Roles of mast cells in rheumatoid arthritis.The Korean journal of internal medicine · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?TH open : companion journal to thrombosis and haemostasis · 2018
    Review
  18. Review
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

A JuurikiviDivision of Rheumatology, Helsinki University Central Hospital, Kasarmikatu 11-13, 00130 Helsinki, Finland.
C Sandler
K A Lindstedt
P T Kovanen
T Juutilainen
M J Leskinen
T Mäki
K K Eklund
Helsinki University Hospital · FIWihuri Research Institute · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMast cells have been implicated in the pathogenesis of arthritis, but elucidation of their precise role has been hampered by a lack of efficient and selective inhibitors of their function.

objectiveTo elucidate the role of mast cells in the pathogenesis of rheumatoid arthritis (RA) and to assess whether apoptosis of cultured and synovial tissue mast cells can be induced by inhibiting mast cell growth factor receptor, c-kit tyrosine kinase. METHODS AND

resultsDouble staining with tumour necrosis factor (TNF) alpha and tryptase antibodies showed the presence of TNFalpha positive mast cells in human rheumatoid synovial tissue. Selective activation of mast cells by anti-IgE resulted in production of TNFalpha in synovial tissue cultures. Inhibition of the c-kit tyrosine kinase with imatinib mesylate (1.0-10 micromol/l) induced profound apoptosis in cultured mast cells as judged by typical apoptotic morphology, increased number of apoptotic nucleosomes, and activation of caspases 8 and 9. Importantly, imatinib also induced apoptosis of mast cells in explant cultures of synovial tissue obtained from patients with RA as judged by a TUNEL assay. Inhibition of c-kit tyrosine kinase was accompanied by significant reduction of TNFalpha production in synovial tissue cultures.

conclusionMast cells may have a role in the pathogenesis of RA, and inhibition of c-kit may be a new means of inhibiting mast cell activity and of abrogating the contribution of mast cells to synovial inflammation in RA.

Indexed as

AnimalsApoptosisArthritis, RheumatoidBenzamidesCells, CulturedDose-Response Relationship, DrugHumansImatinib MesylateMast CellsMiceMice, Inbred BALB CPiperazinesProtein Kinase InhibitorsProto-Oncogene Proteins c-kitPyrimidinesSynovial MembraneBenzamidesImatinib MesylatePiperazinesProtein Kinase InhibitorsProto-Oncogene Proteins c-kitPyrimidinesTumor Necrosis Factor-alpha

Identifiers

PMID16014680
PMCPMC1755598
OpenAlexW2164150729

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.