Evidence map›Paper›PMID 27575371›Full record

ArticlePloS one2016

24R,25-Dihydroxyvitamin D3 Protects against Articular Cartilage Damage following Anterior Cruciate Ligament Transection in Male Rats.

Barbara D Boyan, Sharon L Hyzy, Qingfen Pan, Kayla M Scott, Richard D Coutts, Robert Healey, Zvi Schwartz

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  11. The serum vitamin D metabolome: What we know and what is still to discover.The Journal of steroid biochemistry and molecular biology · 2019
    Review
  12. 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 4 institutions in 1 country.

Barbara D BoyanDepartment of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, Virginia, United States of America.
Sharon L HyzyDepartment of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, Virginia, United States of America.
Qingfen PanSchool of Mechanical Engineering, College of Engineering, Georgia Institute of Technology, Atlanta, Georgia, United States of America.
Kayla M ScottDepartment of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, Virginia, United States of America.
Richard D CouttsDepartment of Orthopedic Surgery, University of California San Diego, San Diego, California, United States of America.
Robert HealeyDepartment of Orthopedic Surgery, University of California San Diego, San Diego, California, United States of America.
Zvi SchwartzDepartment of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, Virginia, United States of America.
Virginia Commonwealth University · USUniversity of California, San Diego · USGeorgia Institute of Technology · USThe Wallace H. Coulter Department of Biomedical Engineering · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) in humans is associated with low circulating 25-hydroxyvitamin D3 [25(OH)D3]. In vitamin D replete rats, radiolabeled 24R,25-dihydroxyvitamin D3 [24R,25(OH)2D3] accumulates in articular cartilage following injection of [3H]-25(OH)D3. Previously, we showed that 24R,25(OH)2D3 blocks chondrocyte apoptosis via phospholipase D and p53, suggesting a role for 24R,25(OH)2D3 in maintaining cartilage health. We examined the ability of 24R,25(OH)2D3 to prevent degenerative changes in articular cartilage in an OA-like environment and the potential mechanisms involved. In vitro, rat articular chondrocytes were treated with IL-1β with and without 24R,25(OH)2D3 or 1α,25(OH)2D3. 24R,25(OH)2D3 but not 1α,25(OH)2D3 blocked the effects of IL-1β in a dose-dependent manner, and its effect was partially mediated through the TGF-β1 signaling pathway. In vivo, unilateral anterior cruciate ligament transections were performed in immunocompetent rats followed by intra-articular injections of 24R,25(OH)2D3 or vehicle (t = 0, 7, 14, 21 days). Tissues were harvested on day 28. Joints treated with vehicle had changes typical of OA whereas joints treated with 24R,25(OH)2D3 had less articular cartilage damage and levels of inflammatory mediators. These results indicate that 24R,25(OH)2D3 protects against OA, and suggest that it may be a therapeutic approach for preventing trauma-induced osteoarthritis.

Indexed as

24,25-Dihydroxyvitamin D 3AnimalsAnterior Cruciate Ligament InjuriesCartilage, ArticularCells, CulturedDisease Models, AnimalDose-Response Relationship, DrugGene Expression RegulationHumansInjections, Intra-ArticularInterleukin-1betaMaleOsteoarthritis, KneeRatsSignal TransductionTransforming Growth Factor beta124,25-Dihydroxyvitamin D 3Interleukin-1betaTgfb1 protein, ratTransforming Growth Factor beta1Vitamins

Identifiers

PMID27575371
PMCPMC5019362
OpenAlexW2510129303

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.