Evidence map›Paper›PMID 26192086›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2015

Endoplasmic reticulum stress as a novel target to ameliorate epithelial-to-mesenchymal transition and apoptosis of human peritoneal mesothelial cells.

Hyun-Soo Shin, Eun-Sun Ryu, Eok-Soo Oh, Duk-Hee Kang

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 47 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Hyun-Soo ShinDepartment of Internal Medicine, Division of Nephrology, Ewha Medical Research Center, School of Medicine, Ewha Womans University, Seoul, Republic of Korea.
Eun-Sun RyuDepartment of Internal Medicine, Division of Nephrology, Ewha Medical Research Center, School of Medicine, Ewha Womans University, Seoul, Republic of Korea.
Eok-Soo OhDepartment of Life Sciences, Division of Life and Pharmaceutical Sciences, Ewha Womans University, Seoul, Republic of Korea.
Duk-Hee KangDepartment of Internal Medicine, Division of Nephrology, Ewha Medical Research Center, School of Medicine, Ewha Womans University, Seoul, Republic of Korea.
Ewha Womans University Medical Center · KREwha Womans University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-to-mesenchymal transition (EMT) and apoptosis of peritoneal mesothelial cells are known to be the earliest mechanisms of peritoneal fibrosis in peritoneal dialysis (PD). Endoplasmic reticulum (ER) stress with an unfolded protein response is regarded to have a role in the development of organ fibrosis. To investigate the potential role of ER stress as a target to prevent and/or delay the development of peritoneal fibrosis, we examined the effect of ER stress on EMT or apoptosis of human peritoneal mesothelial cells (HPMCs) and elucidated the mechanisms underlying the protective effect of ER stress preconditioning on TGF-β1-induced EMT. ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of β-catenin and Snail expression. Low concentrations of TM and TG did not induce apoptosis within 48 h; however, high concentrations of TM- (>1 ng/ml) and TG- (>1 nM) induced apoptosis at 12 h with a persistent increase in C/EBP homologous protein. TGF-β1 induced EMT and apoptosis in HPMCs, which was ameliorated by taurine-conjugated ursodeoxycholic acid, an ER stress blocker. Interestingly, pre-treatment with TM or TG for 4 h also protected the cells from TGF-β1-induced EMT and apoptosis, demonstrating the role of ER stress as an adaptive response to protect HPMCs from EMT and apoptosis. Peritoneal mesothelial cells isolated from PD patients displayed an increase in GRP78/94, which was correlated with the degree of EMT. These findings suggest that the modulation of ER stress in HPMCs could serve as a novel approach to ameliorate peritoneal damage in PD patients.

Indexed as

ApoptosisEndoplasmic Reticulum StressEpithelial-Mesenchymal TransitionModels, BiologicalUnfolded Protein ResponseAnti-Bacterial AgentsAscitic Fluidbeta CateninCells, CulturedEndoplasmic Reticulum Chaperone BiPGene Expression RegulationHumansMembrane Transport ModulatorsNuclear Localization SignalsPeritoneal DialysisPeritoneal FibrosisAnti-Bacterial Agentsbeta CateninCTNNB1 protein, humanEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanMembrane Transport ModulatorsNuclear Localization SignalsSmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanSnail Family Transcription FactorsThapsigarginTranscription FactorsTransforming Growth Factor beta1Tunicamycin

Identifiers

PMID26192086
OpenAlexW1585216184

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.