Evidence map›Paper›PMID 30619956›Full record

ArticleHeliyon2018

Corneal keratin aggresome (CKAGG) formation and clearance by proteasome activation.

Fawzia Bardag-Gorce, Andrew Makalinao, Imara Meepe, Richard H Hoft, Daileen Cortez, Joan Oliva, Amanda Laporte, Jeremy Stark, Amber Gorce, Michael Di Lorenzo and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Heliyon, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. The Role of the Ubiquitin System in Eye Diseases.Life (Basel, Switzerland) · 2025
    Review
  2. 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

13 authors at 1 institution in 1 country.

Fawzia Bardag-GorceLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
Andrew MakalinaoLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
Imara MeepeLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
Richard H HoftLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
Daileen CortezLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
Joan OlivaLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
Amanda LaporteLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
Jeremy StarkLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
Amber GorceLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
Michael Di LorenzoLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
Samuel W FrenchLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
William LungoLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
Yutaka NiiharaLos Angeles BioMedical Research Institute, Torrance, CA, 90502, USA.
The Lundquist Institute · US

Funding

MBRS RISE at CSU Dominguez HillsR25GM062252 · NIGMS · CALIFORNIA STATE UNIV-DOMINGUEZ HILLS · PI MARTINEZ, HERNAN LEONARDO · 2001 to 2020
$7.3M
NIGMS NIH HHS R25 GM062252
6 · The paper itself

Abstract

purposeTo understand the mechanism of corneal keratin expression and clearance in corneal epithelium with Limbal Stem Cell Deficiency (LSCD). The hypothesis is that LSCD-induced proteasome dysfunction is a contributing factor to keratin aggregation, causing corneal keratin aggresome (CKAGG) formation.

methodLSCD was surgically induced in rabbit corneas. LSCD corneal epithelial cells (D-CEC) were collected to investigate keratin K4 and K13 expression and CKAGG formation. Oral mucosal epithelial cells (OMECS) were isolated and cultured to study K4 and K13 expression. Cultured cells were treated with proteasome inhibitor to induce CKAGG formation.

resultsK4 and K13 were strongly expressed in D-CEC, with additional higher molecular weight bands of K4 and K13, suggesting CKAGG formation. Double staining of K4/K13 and ubiquitin showed co-localization of these keratins with ubiquitin in D-CEC. Proteasome inhibition also showed K4/K13 modification and accumulation in cultured OMECS, similar to D-CEC. Proteasome activation was then performed in cultured OMEC. There was no accumulation of keratins, and levels of unmodified keratins were found significantly reduced.

conclusionResults showed an abnormal expression of K4 and K13 after LSCD-induced proteasome dysfunction, which coalesce to form CKAGG in Corneal Epithelial Cells (CEC). We propose that CKAGG formation may be one of the causative factors of morphological alterations in the injured corneal epithelium, and that CKAGG could potentially be cleared by enhancing proteasome activity.

Indexed as

Cell biologyOphthalmology

Identifiers

PMID30619956
PMCPMC6313837
OpenAlexW2904521504

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.