Evidence map›Paper›PMID 28785775›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2017

T3 peptide, a fragment of tumstatin, stimulates proliferation and migration of cardiac fibroblasts through activation of Akt signaling pathway.

Jumpei Yasuda, Kana Fukui, Muneyoshi Okada, Hideyuki Yamawaki

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Extracellular matrix dynamics in vascular remodeling.American journal of physiology. Cell physiology · 2020
    Review
  5. Extracellular matrix-derived peptides in tissue remodeling and fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Review
  6. Article
  7. Extracellular Matrix in Ischemic Heart Disease, Part 4/4: JACC Focus Seminar.Journal of the American College of Cardiology · 2020
    Review
  8. Review
  9. Review
  10. 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

4 authors at 1 institution in 1 country.

Jumpei YasudaLaboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Higashi 23 Bancho 35-1, Towada, Aomori, 034-8628, Japan.
Kana FukuiLaboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Higashi 23 Bancho 35-1, Towada, Aomori, 034-8628, Japan.
Muneyoshi OkadaLaboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Higashi 23 Bancho 35-1, Towada, Aomori, 034-8628, Japan. mokada@vmas.kitasato-u.ac.jp.ORCID http://orcid.org/0000-0002-0746-206X
Hideyuki YamawakiLaboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Higashi 23 Bancho 35-1, Towada, Aomori, 034-8628, Japan.
Kitasato University · JP

Funding

Japan Society for the Promotion of Science JP16J07684
6 · The paper itself

Abstract

Proliferation and migration of cardiac fibroblasts are important in early stage of wound-healing after myocardial infarction. The effects of tumstatin, a cleaved fragment of collagen type IV α3 chain, on these functions of cardiac fibroblasts have not been clarified. In this study, we examined it by using T3 peptide, an active fragment of tumstatin. Cardiac fibroblasts were isolated from ventricles of adult male Wistar rats. Proliferation was examined by a cell counting assay. Boyden chamber assay was performed to examine migration. Expression and phosphorylation of proteins were determined by Western blotting. T3 peptide (300 ng/ml, 24 h) significantly increased proliferation and migration of cardiac fibroblasts. T3 peptide (300 ng/ml, 30 min) significantly increased Akt (Ser473) phosphorylation. LY294002 (10 μM, 30 min pretreatment), a phosphoinositide 3-kinase (PI3K)/Akt inhibitor, significantly inhibited the T3 peptide-induced proliferation, migration, and activation of Akt signaling pathway in cardiac fibroblasts. Cilengitide, an inhibitor of integrin α

Indexed as

AnimalsCell MovementCell ProliferationCells, CulturedChromonesCollagen Type IVFibroblastsMaleMorpholinesMyocardial InfarctionPeptide FragmentsPhosphoinositide-3 Kinase InhibitorsPhosphorylationProto-Oncogene Proteins c-aktRats, Wistar2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesCollagen Type IVMorpholinesPeptide FragmentsPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-akttumstatin (69-88)Cardiac fibroblastsMigrationProliferationTumstatinWound-healing

Identifiers

PMID28785775
OpenAlexW2744547832

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.