Evidence map›Paper›PMID 24042342›Full record

ArticleThe Journal of investigative dermatology2014

siRNA knockdown of tissue inhibitor of metalloproteinase-1 in keloid fibroblasts leads to degradation of collagen type I.

Masayo Aoki, Koichi Miyake, Rei Ogawa, Teruyuki Dohi, Satoshi Akaishi, Hiko Hyakusoku, Takashi Shimada

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Anti-Fibrotic Effects of RF Electric Currents.International journal of molecular sciences · 2023
    Article
  9. Review
  10. siRNA-MediatedInternational journal of molecular sciences · 2023
    Article
  11. Inhibition Effect ofClinical, cosmetic and investigational dermatology · 2023
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Emerging and Novel Therapies for Keloids: A compendious review.Sultan Qaboos University medical journal · 2021
    Review
  17. Article
  18. Targeting metabolic dysregulation for fibrosis therapy.Nature reviews. Drug discovery · 2020
    Review
  19. Article
  20. 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 1 institution in 1 country.

Masayo AokiDivision of Gene Therapy Research Center for Advanced Medical Technology, Department of Biochemistry and Molecular Biology, Tokyo, Japan; Department of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical School, Tokyo, Japan.
Koichi MiyakeDivision of Gene Therapy Research Center for Advanced Medical Technology, Department of Biochemistry and Molecular Biology, Tokyo, Japan. Electronic address: kmiyake@nms.ac.jp.
Rei OgawaDepartment of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical School, Tokyo, Japan.
Teruyuki DohiDivision of Gene Therapy Research Center for Advanced Medical Technology, Department of Biochemistry and Molecular Biology, Tokyo, Japan; Department of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical School, Tokyo, Japan.
Satoshi AkaishiDepartment of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical School, Tokyo, Japan.
Hiko HyakusokuDepartment of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical School, Tokyo, Japan.
Takashi ShimadaDivision of Gene Therapy Research Center for Advanced Medical Technology, Department of Biochemistry and Molecular Biology, Tokyo, Japan.
Nippon Medical School · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Keloids are defined as overgrowths of scar tissue resulting from abnormal wound healing. They are characterized by excessive dermal deposition of thick, hyalinized collagen bundles resulting from an imbalance between the production and degradation of extracellular matrix (ECM) components. Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are two important regulators of ECM degradation and remodeling. To evaluate the role played by knockdown of TIMPs in keloid formation, we transduced human keloid-derived fibroblasts (KFs) with small interfering RNAs targeting TIMP-1 or -2 (siTIMP-1 or siTIMP-2) using a lentiviral vector and assessed the biological effects. We found that MMP-1/TIMP-1 and MMP-1/TIMP-2 complexes were suppressed and that MMP-2 activity was upregulated in KFs expressing siTIMP-1 or siTIMP-2. In addition, increased degradation of collagen type I was observed in the supernatant of KFs expressing siTIMP-1, but not siTIMP-2, with the suppression of cell viability and induction of apoptosis. These results suggest that targeting TIMP-1 using small interfering RNA has significant therapeutic potential as an approach to treating keloids through degradation of their thick collagen bundles.

Indexed as

ApoptosisCollagenasesCollagen Type ICollagen Type I, alpha 1 ChainCollagen Type IIICulture MediaFibroblastsGelatinasesHumansKeloidKeratinocytesPrimary Cell CultureRNA, Small InterferingTissue Inhibitor of Metalloproteinase-1Tissue Inhibitor of Metalloproteinase-2Transduction, GeneticCOL3A1 protein, humanCollagenasesCollagen Type ICollagen Type I, alpha 1 ChainCollagen Type IIICulture MediaGelatinasesRNA, Small InterferingTIMP1 protein, humanTIMP2 protein, humanTissue Inhibitor of Metalloproteinase-1Tissue Inhibitor of Metalloproteinase-2

Identifiers

PMID24042342
OpenAlexW1975755455

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.