Evidence map›Paper›PMID 15972953›Full record

ArticleThe American journal of pathology2005

Tenascin-C regulates recruitment of myofibroblasts during tissue repair after myocardial injury.

Masashi Tamaoki, Kyoko Imanaka-Yoshida, Kazuto Yokoyama, Tomohiro Nishioka, Hiroyasu Inada, Michiaki Hiroe, Teruyo Sakakura, Toshimichi Yoshida

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02767960 (Change of Serum Tenascin-C Concentration and the Relationship With Hs-CRP,cTnI and Prognosis in Patients With Acute Coronary Syndrome), which is not on this map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
4.0field-weighted citation impact, top 6% 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.

NCT02767960 completednot on this mapstarted 2016, after this paper: background citation

Change of Serum Tenascin-C Concentration and the Relationship With Hs-CRP,cTnI and Prognosis in Patients With Acute Coronary Syndrome

Typeobservational_patient_registrySponsorThe First Affiliated Hospital of Dalian Medical UniversityRan2016 to 2017Enrolled183ConditionsAcute Coronary Syndrome
3 · Its place in the literature

Who cites it

95 citing papers in PubMed, 197 citations in OpenAlex.

  1. Tenascin CNature communications · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Tenascin-C in Tissue Repair after Myocardial Infarction in Humans.International journal of molecular sciences · 2023
    Article
  13. Review
  14. Article
  15. TGF-β in developmental and fibrogenic EMTs.Seminars in cancer biology · 2022
    Review
  16. Article
  17. Tenascin-C in fibrosis in multiple organs: Translational implications.Seminars in cell & developmental biology · 2022
    Review
  18. Review
  19. Article
  20. Tenascin-C in Heart Diseases-The Role of Inflammation.International journal of molecular sciences · 2021
    Review

35 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Masashi TamaokiDepartment of Pathology and Biology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Kyoko Imanaka-Yoshida
Kazuto Yokoyama
Tomohiro Nishioka
Hiroyasu Inada
Michiaki Hiroe
Teruyo Sakakura
Toshimichi Yoshida
Mie University · JPSaitama International Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tenascin-C (TN-C) is an extracellular matrix molecule that is expressed during wound healing in various tissues. Although not detectable in the normal adult heart, it is expressed under pathological conditions. Previously, using a rat model, we found that TN-C was expressed during the acute stage after myocardial infarction and that alpha-smooth muscle actin (alpha-SMA)-positive myofibroblasts appeared in TN-C-positive areas. In the present study, we examined whether TN-C controls the dynamics of myofibroblast recruitment and wound healing after electrical injury to the myocardium of TN-C knockout (TNKO) mice compared with wild-type (WT) mice. In TNKO mice, myocardial repair seemed to proceed normally, but the appearance of myofibroblasts was delayed. With cultured cardiac fibroblasts, TN-C significantly accelerated cell migration, alpha-SMA expression, and collagen gel contraction but did not affect proliferation. Using recombinant fragments of murine TN-C, the functional domain responsible for promoting migration of cardiac fibroblasts was mapped to the conserved fibronectin type III (FNIII)-like repeats and the fibrinogen (Fbg)-like domain. Furthermore, alternatively spliced FNIII and Fbg-like domains proved responsible for the up-regulation of alpha-SMA expression. These results indicate that TN-C promotes recruitment of myofibroblasts in the early stages of myocardial repair by stimulating cell migration and differentiation.

Indexed as

AnimalsCell DifferentiationCell MovementCell ProliferationFibroblastsHeart InjuriesImmunohistochemistryMiceMice, KnockoutMyocardiumRatsRecombinant ProteinsTenascinWound HealingRecombinant ProteinsTenascin

Identifiers

PMID15972953
PMCPMC1603439
OpenAlexW1986722306

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.