Evidence map›Paper›PMID 32204600›Full record

ArticleCartilage2021

TNIIIA2, The Peptide of Tenascin-C, as a Candidate for Preventing Articular Cartilage Degeneration.

Tetsuya Hattori, Masahiro Hasegawa, Hironori Unno, Takahiro Iino, Fumio Fukai, Toshimichi Yoshida, Akihiro Sudo

Open access · bronzeAbstract read
In one paragraph

Article in Cartilage, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
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  4. Review
  5. 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

7 authors at 2 institutions in 1 country.

Tetsuya HattoriDepartment of Orthopaedic Surgery, Mie University Graduate School of Medicine, Tsu City, Mie, Japan.
Masahiro HasegawaDepartment of Orthopaedic Surgery, Mie University Graduate School of Medicine, Tsu City, Mie, Japan.ORCID 0000-0001-7948-2003
Hironori UnnoDepartment of Orthopaedic Surgery, Mie University Graduate School of Medicine, Tsu City, Mie, Japan.
Takahiro IinoDepartment of Orthopaedic Surgery, Mie University Graduate School of Medicine, Tsu City, Mie, Japan.
Fumio FukaiDepartment of Molecular Patho-Physiology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda City, Chiba, Japan.
Toshimichi YoshidaDepartments of Pathology & Matrix Biology, Mie University Graduate School of Medicine, Tsu City, Mie, Japan.ORCID 0000-0001-8935-8217
Akihiro SudoDepartment of Orthopaedic Surgery, Mie University Graduate School of Medicine, Tsu City, Mie, Japan.
Mie University · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTNIIIA2 is a peptide of the extracellular matrix glycoprotein tenascin-C. We evaluated whether intra-articular injection of TNIIIA2 could prevent articular cartilage degeneration without inducing synovitis in an osteoarthritis mice model.

designTen micrograms per milliliter of TNIIIA2 were injected into the knee joint of mice (group II) to evaluate the induction of synovitis. The control group received an injection of phosphate buffered saline (group I). Synovitis was evaluated using synovitis score 2 and 4 weeks after injection. The ligaments of knee joints of mice were transected to make the osteoarthritis model. After transection, 10 µg/mL of TNIIIA2 was injected into the knee joint (group IV). The control group received an injection of phosphate buffered saline after transection (group III). Histologic examinations were made using hematoxylin and eosin and safranin-O staining at 2, 4, 8, and 12 weeks postoperatively. An

resultsThere were no differences between groups in the study of intra-articular injection of mice (group I vs. group II). In the osteoarthritis model, we found development of osteoarthritis was suppressed in group IV at 4 and 8 weeks. TNIIIA2 upregulated the expressions of tumor necrosis factor-α, matrix metalloproteinase 3, and basic fibroblast growth factor.

conclusionWe demonstrated that TNIIIA2 could prevent cartilage degeneration without synovitis.

Indexed as

Cartilage, ArticularCartilage DiseasesAnimalsExtracellular MatrixMicePeptidesTenascinPeptidesTenascinmouse modelosteoarthritissynovitistenascin-CTNIIIA2

Identifiers

PMID32204600
PMCPMC8804811
OpenAlexW3012621059

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.