Evidence map›Paper›PMID 30648255›Full record

ArticleJournal of cellular physiology2019

The Smad2/3/4 complex binds miR-139 promoter to modulate TGFβ-induced proliferation and activation of human Tenon's capsule fibroblasts through the Wnt pathway.

Mi Deng, Shi-Ying Hou, Bo-Ding Tong, Jia-Yang Yin, Wei Xiong

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Wound Modulations in Glaucoma Surgery: A Systematic Review.Bioengineering (Basel, Switzerland) · 2024
    Review
  6. Review
  7. Involvement of METTL3/mJournal of molecular histology · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

5 authors at 1 institution in 1 country.

Mi DengDepartment of Ophthalmology, Hunan Clinical Research Center of Ophthalmic Disease, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Shi-Ying HouDepartment of Ophthalmology, Hunan Clinical Research Center of Ophthalmic Disease, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Bo-Ding TongDepartment of Ophthalmology, Hunan Clinical Research Center of Ophthalmic Disease, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jia-Yang YinDepartment of Ophthalmology, Hunan Clinical Research Center of Ophthalmic Disease, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Wei XiongDepartment of Ophthalmology, Hunan Clinical Research Center of Ophthalmic Disease, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.ORCID 0000-0002-3017-9895
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The activation and proliferation of human Tenon's fibroblasts (HTFs) play a vital role in the fibrosis in the pathology of the scar formation after the glaucoma filtration surgery. Transforming growth factor β1 (TGFβ1)/Smads signaling has been reported to promote fibrosis. In our previous study, we revealed that TGFβ1-induced orbital fibroblast activation and proliferation through Wnt/β-catenin signaling. As microRNA (miR)-139 could target several factors in Wnt signaling to modulate fibrosis, here, the effect and mechanism of miR-139 in HTF activation and proliferation were investigated. miR-139 overexpression significantly reversed the TGFβ1-induced increase in collagen I and α-smooth muscle actin contents and proliferation in HTFs. CTNNB1 and CTNND1 were direct downstream of miR-139 and can significantly restore the suppressive effect of miR-139 on the activation and proliferation in HTFs under TGFβ1 stimulation. Smad2/3/4 complex inhibits the transcription activity of miR-139, most possibly by Smad4 binding to the miR-139 promoter. Taken together, we demonstrated a new mechanism of HTF activation and proliferation from the perspective of miRNA regulation, which may provide new strategies for improving the fibrosis after the glaucoma filtration surgery.

Indexed as

beta CateninBinding SitesCateninsCell ProliferationCicatrixDelta CateninFibroblastsFibrosisGlaucoma Drainage ImplantsHumansMicroRNAsPromoter Regions, GeneticSmad2 ProteinSmad3 ProteinSmad4 ProteinSmad Proteinsbeta CateninCateninsCTNNB1 protein, humanDelta CateninMicroRNAsMIRN139 microRNA, humanSmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanSmad4 ProteinSMAD4 protein, humanSmad ProteinsTGFB1 protein, humanTransforming Growth Factor beta1human Tenon's fibroblasts (HTFs)miR-139proliferationSmad2/3/4 complexTGFβ1

Identifiers

PMID30648255
PMCPMC13483270
OpenAlexW2911067598

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.