Evidence map›Paper›PMID 12932288›Full record

ArticleArthritis research & therapy2003

Higher susceptibility to Fas ligand induced apoptosis and altered modulation of cell death by tumor necrosis factor-alpha in periarticular tenocytes from patients with knee joint osteoarthritis.

Andreas Machner, Anja Baier, Aline Wille, Susanne Drynda, Géza Pap, Andreas Drynda, Christian Mawrin, Frank Bühling, Steffen Gay, Wolfram Neumann and 1 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Arthritis research & therapy, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
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  9. Lose-Dose Administration of Dexamethasone Is Beneficial in Preventing Secondary Tendon Damage in a Stress-Deprived Joint Injury Explant Model.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020
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  18. Reactive oxygen species and tendinopathy: do they matter?British journal of sports medicine · 2004
    Review
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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

11 authors at 2 institutions in 2 countries.

Andreas MachnerDepartment of Orthopedic Surgery, Otto-von-Guericke-University, Magdeburg, Germany.
Anja Baier
Aline Wille
Susanne Drynda
Géza Pap
Andreas Drynda
Christian Mawrin
Frank Bühling
Steffen Gay
Wolfram Neumann
Thomas Pap
Otto-von-Guericke University Magdeburg · DEUniversity Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to investigate the expression of Fas in periarticular tenocytes of patients with osteoarthritis (OA) and to study their susceptibility to Fas ligand-mediated apoptosis. Tendon samples were obtained from the quadriceps femoris muscle of patients with knee OA and used for histological evaluation, for immunohistochemical detection of Fas, and to establish tenocyte cultures. The expression of Fas mRNA was determined by quantitative PCR. Levels of soluble Fas and soluble tumour necrosis factor (TNF) receptor I were measured using ELISA. Apoptosis was induced with recombinant human Fas ligand and measured by a histone fragmentation assay and flow cytometry. The effects of TNF-alpha were studied by stimulation with TNF-alpha alone or 24 hours before the induction of apoptosis. Tendon samples from non-OA patients were used as controls. Histological evaluation revealed degenerative changes in the tendons of all OA patients but not in the controls. Fas was detected by immunohistochemistry in all specimens, but quantitative PCR revealed significantly higher levels of Fas mRNA in OA tenocytes. In contrast, lower levels of soluble Fas were found in OA tenocytes by ELISA. OA tenocytes were significantly more susceptible to Fas ligand induced apoptosis than were control cells. TNF-alpha reduced the Fas ligand induced apoptosis in OA tenocytes but had no effects on control tenocytes. These data suggest that knee OA is associated with higher susceptibility of periarticular tenocytes to Fas ligand induced apoptosis because of higher expression of Fas but lower levels of apoptosis-inhibiting soluble Fas. These changes may contribute to decreased cellularity in degenerative tendons and promote their rupturing. The antiapoptotic effects of TNF-alpha in OA tenocytes most likely reflect regenerative attempts and must be taken into account when anti-TNF strategies are considered for OA.

Indexed as

ApoptosisArthroplasty, Replacement, KneeCell DeathFas Ligand Proteinfas ReceptorFemurHumansKnee JointMembrane GlycoproteinsMuscle, SkeletalOsteoarthritis, KneeRNA, MessengerSolubilityTendonsTumor Necrosis Factor-alphaFASLG protein, humanFas Ligand Proteinfas ReceptorMembrane GlycoproteinsRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID12932288
PMCPMC193726
OpenAlexW2102892310

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.