Evidence map›Paper›PMID 30902076›Full record

ArticleBMC musculoskeletal disorders2019

Molecular changes to tendons after collagenase-induced acute tendon injury in a senescence-accelerated mouse model.

Yasuhiro Ueda, Atsuyuki Inui, Yutaka Mifune, Fumiaki Takase, Takeshi Kataoka, Takashi Kurosawa, Kohei Yamaura, Takeshi Kokubu, Ryosuke Kuroda

Abstract read
In one paragraph

Article in BMC musculoskeletal disorders, 2019. 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
–field-weighted citation impact
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.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Reparative and Maladaptive Inflammation in Tendon Healing.Frontiers in bioengineering and biotechnology · 2021
    Review
  10. In Vitro Innovation of Tendon Tissue Engineering Strategies.International journal of molecular sciences · 2020
    Review
  11. Article
  12. Models of tendon development and injury.BMC biomedical engineering · 2019
    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

9 authors.

Yasuhiro UedaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, chuo-ku, Kobe, 650-0017, Japan.
Atsuyuki InuiDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, chuo-ku, Kobe, 650-0017, Japan.
Yutaka MifuneDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, chuo-ku, Kobe, 650-0017, Japan. m-ship@kf7.so-net.ne.jp.
Fumiaki TakaseDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, chuo-ku, Kobe, 650-0017, Japan.
Takeshi KataokaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, chuo-ku, Kobe, 650-0017, Japan.
Takashi KurosawaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, chuo-ku, Kobe, 650-0017, Japan.
Kohei YamauraDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, chuo-ku, Kobe, 650-0017, Japan.
Takeshi KokubuDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, chuo-ku, Kobe, 650-0017, Japan.
Ryosuke KurodaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, chuo-ku, Kobe, 650-0017, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAging impairs tendon healing and is a potential risk factor for chronic tendinitis. During normal aging, tendons undergo structural and biomechanical degenerative changes, accompanied by a reduction in the number of tenocytes and changes to their properties. However, molecular changes in aged tendons under inflammatory conditions are not well understood. The present study analyzed the molecular changes in collagenase induced acute tendon injury using a senescence-accelerated mouse (SAM) model.

methodsSAMP6 mice were used as an aging animal model and SAMR1 mice were used as a control to represent a senescence-resistant inbred strain. All the mice used in the study were 40 weeks old. Collagenase I from Clostridium histolyticum (20 μL) was injected percutaneously to the tendon-bone junction of the Achilles tendon. Two weeks after treatment, the Achilles tendons were harvested and stained using Picrosirius Red to determine collagen expression. Real-time PCR was performed to analyze gene expression of IL-6, tenomodulin, type I and type II collagen, MMP-9, TIMP-1, and TIMP-2.

resultsCollagenase injection resulted in significantly higher gene expression of IL-6 but significantly lower tenomodulin expression compared with the control in SAMP6 and SAMR1 mice. In SAMP6 mice, gene expression of type III collagen and MMP-9 was significantly higher in the collagenase-injected group compared with the control group. SAMP6 mice also showed lower expression of type I collagen, TIMP-1, and TIMP-2 in the collagenase-injected group compared with the control group. Picrosirius Red staining showed the highest expression of type III collagen in the collagenase-injected SAMP6 group compared with the other groups.

conclusionsThe collagenase-injected SAMP6 group showed higher expression of IL-6, MMP-9, and type III collagen and lower expression of type I collagen, TIMP-1, and TIMP-2, which are known to suppress metalloproteinases. The results indicate that aging may lead to dysfunction of the tendon healing process after acute tendon injury.

Indexed as

Disease Models, AnimalAgingAnimalsCollagenasesMaleMembrane ProteinsMiceMice, TransgenicNuclear ProteinsTendon InjuriesCollagenasesMembrane ProteinsNuclear ProteinsSamp1 protein, mouseAcute tendon injuryAgingTendon degeneration

Identifiers

PMID30902076
PMCPMC6429773

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Registered trials

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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.