Evidence map›Paper›PMID 29242028›Full record

ArticleExperimental eye research2018

Blockade of KCa3.1: A novel target to treat TGF-β1 induced conjunctival fibrosis.

Govindaraj Anumanthan, Philip J Wilson, Ratnakar Tripathi, Nathan P Hesemann, Rajiv R Mohan

Open access · greenAbstract read
In one paragraph

Article in Experimental eye research, 2018. 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
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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  8. Involvement of METTL3/mJournal of molecular histology · 2021
    Article
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  10. 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

5 authors at 1 institution in 1 country.

Govindaraj AnumanthanVeterinary Medicine and Surgery, University of Missouri, Columbia, MO, United States; Harry S. Truman Memorial Veteran Hospital, Columbia, MO, United States.
Philip J WilsonMason Eye Institute, School of Medicine, Columbia, MO, United States.
Ratnakar TripathiVeterinary Medicine and Surgery, University of Missouri, Columbia, MO, United States; Harry S. Truman Memorial Veteran Hospital, Columbia, MO, United States.
Nathan P HesemannHarry S. Truman Memorial Veteran Hospital, Columbia, MO, United States; Mason Eye Institute, School of Medicine, Columbia, MO, United States.
Rajiv R MohanVeterinary Medicine and Surgery, University of Missouri, Columbia, MO, United States; Harry S. Truman Memorial Veteran Hospital, Columbia, MO, United States; Mason Eye Institute, School of Medicine, Columbia, MO, United States. Electronic address: mohanr@health.missouri.edu.
Harry S. Truman Memorial Veterans' Hospital · US

Funding

Gene Therapy in the CorneaR01EY017294 · NEI · UNIVERSITY OF MISSOURI-COLUMBIA · PI MOHAN, RAJIV RAVINDRA · 2007 to 2018
$4.3M
Novel approaches for corneal haze/fibrosis eliminationR01EY030774 · NEI · UNIVERSITY OF MISSOURI-COLUMBIA · PI MOHAN, RAJIV RAVINDRA · 2019 to 2022
$1.5M
BLRD VA I01 BX000357BLRD VA IK6 BX005646NEI NIH HHS R01 EY017294NEI NIH HHS R01 EY030774
6 · The paper itself

Abstract

Postoperative conjunctival fibrosis is common in patients after glaucoma filtration surgery. The calcium activated potassium (KCa3.1) channel has been shown to inhibit fibrosis in many non-ocular tissues. However, its potential in treating ocular fibrosis remains unknown. We tested the anti-fibrotic potential of TRAM34, a selective blocker of KCa3.1 channel, in treating conjunctival fibrosis. Primary human conjunctival fibroblast (HCF) cultures derived from donor tissues. Myofibroblasts causing conjunctival fibrosis were generated by growing HCFs in the presence of TGFβ1 for 72 h. KCa3.1 mRNA and protein expression in HCF was examined with PCR and western blot. The anti-fibrotic potential of TRAM34 was examined by measuring fibrotic gene expression with quantitative PCR (qPCR), immunofluorescence, and western blotting in HCFs in ± TGFβ1 (5 ng/ml) and TRAM34 (0-25 μM). The cytotoxicity of Tram34 was analyzed with trypan blue assay and its role in Smad signaling was studied with immunofluorescence. Expression of KCa3.1 mRNA and protein was detected in HCFs and TGFβ1 treatment to HCFs significantly increased expression of KCa3.1. TRAM34 treatment attenuated transcription of fibrotic markers, αSMA (p < .001), fibronectin (p < .05), collagen I (p < .001) and collagen IV (p < .001) in TGFβ1-induced HCFs. Further, TRAM34 significantly inhibited TGFβ1-stimulated αSMA protein expression (p < .01) and nuclear translocation of fibrotic Smad2/3 in HCFs and showed no significant cytotoxicity (p < .05). The KCa3.1 potassium channel plays a significant role in the prevention of conjunctival fibrosis and TRAM34 has potential to control post surgical bleb fibrosis in patients. In vivo studies are warranted.

Indexed as

Blotting, WesternCell ProliferationCells, CulturedConjunctivaFibroblastsFibrosisFluorescent Antibody Technique, IndirectHumansIntermediate-Conductance Calcium-Activated Potassium ChannelsPyrazolesReal-Time Polymerase Chain ReactionRNA, MessengerSmad2 ProteinSmad3 ProteinTransforming Growth Factor beta1Intermediate-Conductance Calcium-Activated Potassium ChannelsKCNN4 protein, humanPyrazolesRNA, MessengerSmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanTRAM 34Transforming Growth Factor beta1

Identifiers

PMID29242028
PMCPMC9250277
OpenAlexW2771780689

What OpenQuestion holds

Textmetadata
LicenceTDM
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.