Evidence map›Paper›PMID 26373710›Full record

ArticleArthritis research & therapy2015

The inhibitory effects of a RANKL-binding peptide on articular and periarticular bone loss in a murine model of collagen-induced arthritis: a bone histomorphometric study.

Genki Kato, Yasuhiro Shimizu, Yuki Arai, Natsuki Suzuki, Yasutaka Sugamori, Miki Maeda, Mariko Takahashi, Yukihiko Tamura, Noriyuki Wakabayashi, Ramachandran Murali and 4 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. RANKL biology.Bone · 2022
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Recent Advances in Osteoclast Biological Behavior.Frontiers in cell and developmental biology · 2021
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

14 authors at 2 institutions in 2 countries.

Genki KatoDepartment of Pharmacology, Division of Bio-Matrix, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. kat-hpha@tmd.ac.jp.
Yasuhiro ShimizuDepartment of Orthodontic Science, Division of Oral Health Sciences, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. y.shimizu.orts@tmd.ac.jp.
Yuki AraiDepartment of Removable Partial Prosthodontics, Division of Oral Health Science, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. y.arai.rpro@tmd.ac.jp.
Natsuki SuzukiDepartment of Removable Partial Prosthodontics, Division of Oral Health Science, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. naturpro@tmd.ac.jp.
Yasutaka SugamoriDepartment of Pharmacology, Division of Bio-Matrix, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. sug-hpha@tmd.ac.jp.
Miki MaedaDepartment of Pharmacology, Division of Bio-Matrix, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. m.maeda@uke.de.
Mariko TakahashiDepartment of Pharmacology, Division of Bio-Matrix, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. takahashi.hpha@tmd.ac.jp.
Yukihiko TamuraDepartment of Pharmacology, Division of Bio-Matrix, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. tamu.hpha@tmd.ac.jp.
Noriyuki WakabayashiDepartment of Removable Partial Prosthodontics, Division of Oral Health Science, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. wakabayashi.rpro@tmd.ac.jp.
Ramachandran MuraliDepartment of Biomedical Sciences, Research Division of Immunology, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA. Ramachandran.Murali@csmc.edu.
Takashi OnoDepartment of Orthodontic Science, Division of Oral Health Sciences, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. t.ono.orts@tmd.ac.jp.
Keiichi OhyaDepartment of Pharmacology, Division of Bio-Matrix, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. kohya.hpha@tmd.ac.jp.
Setsuko Mise-OmataDepartment of Pharmacology, Division of Bio-Matrix, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. mis-hpha@tmd.ac.jp.
Kazuhiro AokiDepartment of Pharmacology, Division of Bio-Matrix, Graduate School, Tokyo Medical and Dental University, Tokyo, 113-8549, Japan. kazu.hpha@tmd.ac.jp.
Tokyo Medical and Dental University · JPCedars-Sinai Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionWe designed OP3-4 (YCEIEFCYLIR), a cyclic peptide, to mimic the soluble osteoprotegerin (OPG), and was proven to bind to RANKL (receptor activator of NF-κB ligand), thereby inhibiting osteoclastogenesis. We recently found that another RANKL binding peptide, W9, could accelerate bone formation by affecting RANKL signaling in osteoblasts. We herein demonstrate the effects of OP3-4 on bone formation and bone loss in a murine model of rheumatoid arthritis.

methodsTwenty-four seven-week-old male DBA/1J mice were used to generate a murine model of collagen-induced arthritis (CIA). Then, vehicle or OP3-4 (9 mg/kg/day or 18 mg/kg/day) was subcutaneously infused using infusion pumps for three weeks beginning seven days after the second immunization. The arthritis score was assessed, and the mice were sacrificed on day 49. Thereafter, radiographic, histological and biochemical analyses were performed.

resultsThe OP3-4 treatment did not significantly inhibit the CIA-induced arthritis, but limited bone loss. Micro-CT images and quantitative measurements of the bone mineral density revealed that 18 mg/kg/day OP3-4 prevented the CIA-induced bone loss at both articular and periarticular sites of tibiae. As expected, OP3-4 significantly reduced the CIA-induced serum CTX levels, a marker of bone resorption. Interestingly, the bone histomorphometric analyses using undecalcified sections showed that OP3-4 prevented the CIA-induced reduction of bone formation-related parameters at the periarticular sites.

conclusionThe peptide that mimicked OPG prevented inflammatory bone loss by inhibiting bone resorption and stimulating bone formation. It could therefore be a useful template for the development of small molecule drugs for inflammatory bone loss.

Indexed as

Amino Acid SequenceAnimalsArthritis, ExperimentalArthritis, RheumatoidBone DensityBone ResorptionCartilage, ArticularCell DifferentiationCells, CulturedCollagen Type IEnzyme-Linked Immunosorbent AssayInfusions, SubcutaneousMaleMice, Inbred DBAOligopeptidesOsteoblastsCollagen Type Icollagen type I trimeric cross-linked peptideOligopeptidesOP3-4 peptideOsteoprotegerinPeptidesRANK Ligand

Identifiers

PMID26373710
PMCPMC4570694
OpenAlexW2165050339

What OpenQuestion holds

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LicenceCC BY
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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.