Evidence map›Paper›PMID 25917638›Full record

ArticleOsteoarthritis and cartilage2015

Meniscus is more susceptible than cartilage to catabolic and anti-anabolic effects of adipokines.

J F Nishimuta, M E Levenston

Open access · greenAbstract read
In one paragraph

Article in Osteoarthritis and cartilage, 2015. 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
2.2field-weighted citation impact, top 12% 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, 27 citations in OpenAlex.

  1. Article
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  7. Article
  8. Article
  9. Observational
  10. Molecular biology of meniscus pathology: Lessons learned from translational studies and mouse models.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020
    Review
  11. The Adipokine Network in Rheumatic Joint Diseases.International journal of molecular sciences · 2019
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. 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

2 authors at 1 institution in 1 country.

J F NishimutaDepartment of Mechanical Engineering, Stanford University, Stanford, CA 94305, USA. Electronic address: j.nishimuta@gmail.com.
M E LevenstonDepartment of Mechanical Engineering, Stanford University, Stanford, CA 94305, USA; Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. Electronic address: levenston@stanford.edu.
Stanford University · US

Funding

Spatiotemporal Progression of Meniscal DegradationR01AR052861 · NIAMS · STANFORD UNIVERSITY · PI LEVENSTON, MARC ELLIOT · 2005 to 2010
$1.6M
NIAMS NIH HHS R01 AR052861NIAMS NIH HHS R01AR052861
6 · The paper itself

Abstract

objectiveThis study compared the effects on cartilage and meniscus matrix catabolism and biosynthesis of several adipokines implicated in osteoarthritis (OA).

designBovine cartilage and meniscus explants were cultured for 1 or 9 days in serum-free medium alone or with 0.02, 0.2, or 2 μg/ml of leptin, visfatin, adiponectin, or resistin. Media were supplemented with (3)H-proline or (35)S-sodium sulfate to evaluate protein and sulfated glycosaminoglycan (sGAG) accumulation on the last day of culture. Explants were assayed for radiolabel, sGAG, and DNA contents. Cultured media were assayed for sGAG, nitrite and lactate dehydrogenase.

resultsCartilage tissue was minimally affected by adipokines, with only the highest resistin dose increasing sGAG release and nitrite production compared to controls. In sharp contrast, meniscus tissue was responsive to several adipokines, with elevated sGAG and nitrite release following treatment with resistin, leptin, or visfatin. Cartilage sGAG content was unaltered by adipokine treatment whereas meniscal sGAG content significantly decreased with resistin dosage. Protein ((3)H) incorporation was unaffected by adipokine treatment in both tissues. sGAG ((35)S) incorporation did not significantly vary with adipokine treatment in cartilage but was inhibited by treatment with leptin, visfatin, and resistin in meniscus.

conclusionOur results indicate that meniscal tissue is more susceptible to adipokine-stimulated catabolism than is cartilage. Resistin had the strongest effect of the adipokines tested, inducing sGAG release in both tissues and depleting sGAG content in meniscus. These results suggest that increased adipokine levels due to obesity or joint injury may alter the mechanical integrity of the knee joint through biological pathways.

Indexed as

AdipokinesAnimalsCartilage, ArticularCattleDNAGlycosaminoglycansIn Vitro TechniquesLeptinMenisci, TibialProtein BiosynthesisProteinsResistinA73025AdipokinesDNAGlycosaminoglycansLeptinProteinsResistinAdipokinesCartilageDegenerationMeniscusObesityOsteoarthritis

Identifiers

PMID25917638
PMCPMC4558246
OpenAlexW2088029245

What OpenQuestion holds

Textmetadata
LicenceTDM
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.