Evidence map›Paper›PMID 32182995›Full record

ArticleInternational journal of molecular sciences2020

Chondroitin Sulfate Promotes the Proliferation of Keloid Fibroblasts Through Activation of the Integrin and Protein Kinase B Pathways.

Yasuhiro Katayama, Motoko Naitoh, Hiroshi Kubota, Satoko Yamawaki, Rino Aya, Toshihiro Ishiko, Naoki Morimoto

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. 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

7 authors at 6 institutions in 1 country.

Yasuhiro KatayamaDepartment of Plastic Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin-Kawaharacho, Sakyo-ku, Kyoto City, Kyoto 606-8507, Japan.ORCID 0000-0003-1218-9130
Motoko NaitohDepartment of Plastic Surgery, Kobe City Medical Center General Hospital, 2-2-1, Minatojimaminamimachi, Chuo-ku, Kobe City, Hyogo 650-0047, Japan.
Hiroshi KubotaDepartment of Life Science, Faculty of Engineering Science, Akita University, 1-1 Tegata Gakuenmachi, Akita 010-8502, Japan.
Satoko YamawakiDepartment of Plastic and Reconstructive Surgery, Japanese Red Cross Fukui Hospital, 2-4-1, Tsukimi, Fukui City, Fukui 918-8501, Japan.
Rino AyaDepartment of Plastic Surgery, Kyoto Katsura Hospital, 17-banchi, Yamada Hirao-cho, Nishikyo-ku, Kyoto-shi, Kyoto 615-8256, Japan.
Toshihiro IshikoDepartment of Plastic Surgery, Japanese Red Cross Otsu Hospital, 1-1-35, Nagara, Otsu City, Shiga 520-0000, Japan.
Naoki MorimotoDepartment of Plastic Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin-Kawaharacho, Sakyo-ku, Kyoto City, Kyoto 606-8507, Japan.
Kyoto University · JPAkita University · JPFukui Red Cross Hospital · JPKyoto Katsura Hospital · JPOtsu Red Cross Hospital · JPRIKEN Center for Computational Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Keloids are dermal fibroproliferative tumors that arise beyond the boundary of the original wound edges and invades adjacent tissue. Keloids are characterized by the extensive production of extracellular matrix (ECM) and abnormal fibroblast proliferation. Chondroitin sulfate (CS) is one of the major structural components of cartilage and ECM. Recently, we reported the over-accumulation of CS in keloid lesions. Keloid-derived fibroblasts (KFs) and normal dermal fibroblasts (NFs) were incubated with CS. The fibroblast proliferation rate was analyzed using a tetrazolium salt colorimetric assay. The activation of the intracellular signaling pathway was analyzed by Western blotting. Wortmannin, a PI3K inhibitor, and anti-integrin antibodies were tested to investigate the mechanism of the CS-induced cell proliferation. CS strongly stimulated the proliferation of KFs, but not NFs. The analysis of the intracellular signal transduction pathway revealed that the stimulation effect of CS on KF proliferation was due to the activation of the protein kinase B (AKT) pathway and that integrin α1 was responsible for this phenomenon. We revealed that CS probably activates the AKT pathway through integrin to induce KF proliferation. CS may be a novel clinical therapeutic target in keloids.

Indexed as

Cell ProliferationAdultAgedAged, 80 and overCells, CulturedChondroitin SulfatesFemaleFibroblastsHumansIntegrinsKeloidMaleMiddle AgedPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionChondroitin SulfatesIntegrinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktchondroitin sulfatefibroblastintegrinkeloidsPI3K/Akt pathway

Identifiers

PMID32182995
PMCPMC7139995
OpenAlexW3011923657

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.