Evidence map›Paper›PMID 28120575›Full record

ArticleYonsei medical journal2017

Role of TGFBIp in Wound Healing and Mucin Expression in Corneal Epithelial Cells.

Yong Sun Maeng, Ga Hyun Lee, Boram Lee, Seung Il Choi, Tae Im Kim, Eung Kweon Kim

Open access · goldAbstract read
In one paragraph

Article in Yonsei medical journal, 2017. 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
2.7field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Modulation of Epithelial to Mesenchymal Transition Signaling Pathways byInternational journal of molecular sciences · 2019
    Review
  10. Review
  11. Article
  12. 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

6 authors at 2 institutions in 1 country.

Yong Sun MaengDepartment of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Ga Hyun LeeDepartment of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Boram LeeDepartment of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Seung Il ChoiDepartment of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Tae Im KimDepartment of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Eung Kweon KimDepartment of Ophthalmology, Corneal Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Yonsei University · KRSeverance Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTransforming growth factor-β-induced protein (TGFBIp) is highly expressed in the cornea, and mutant TGFBIp induces corneal diseases. However, the function of TGFBIp in cornea epithelium is not fully investigated. Here, we tested the importance of TGFBIp in regulation of gene expression and corneal epithelial cell (CEC) activity. MATERIALS AND

methodsThe effect of TGFBIp on CEC activity was analyzed by cell migration, adhesion, proliferation and wound healing assay. Analysis of gene expression was examined by western blot and quantitative reverse transcription PCR.

resultsThe results demonstrated that TGFBIp increased adhesion, migration, proliferation, and wound healing of CECs. Analysis of gene expression presented that TGFBIp-stimulated CECs exhibited increased expression of mucin family genes, such as MUC1, -4, -5AC, and -16. Furthermore, TGFBIp treatment increased the expression of MUC1, -4, -5AC, -7, and -16 in conjunctival epithelial cells. TGFBIp also increased the activity of intracellular signaling molecules ERK and AKT in CECs. Using pharmacologic inhibitors of ERK and AKT, we showed that the expression of mucin genes by TGFBIp is mediated by the activation of ERK and AKT signaling.

conclusionOur findings demonstrate that the locally generated TGFBIp in the cornea may contribute to wound healing of CECs by enhancing the migration, adhesion, and proliferation of CECs. In addition, our results suggest that TGFBIp has a protective effect on ocular surfaces by inducing the expression of mucin genes in corneal and conjunctival epithelial cells. These data suggest that TGFBIp is a useful therapeutic target for patients with corneal wounds.

Indexed as

betaIG-H3 ProteinBlotting, WesternCell AdhesionCell MovementCell ProliferationCells, CulturedConjunctivaCorneaEpithelial CellsExtracellular Matrix ProteinsGene ExpressionHumansMucinsSignal TransductionTransforming Growth Factor betaWound HealingbetaIG-H3 ProteinExtracellular Matrix ProteinsMucinsTransforming Growth Factor betacorneaepithelial cellsmucinTGFBIp

Identifiers

PMID28120575
PMCPMC5290024
OpenAlexW2580176402

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.