Evidence map›Paper›PMID 27311010›Full record

ArticlePloS one2016

Propofol Decreases Endoplasmic Reticulum Stress-Mediated Apoptosis in Retinal Pigment Epithelial Cells.

Xuezhi Zhou, Yantao Wei, Suo Qiu, Yue Xu, Ting Zhang, Shaochong Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. 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
1.3field-weighted citation impact, top 22% 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, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Propofol Induces the Expression of Nrf2 and HO-1 inTropical medicine and infectious disease · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Impact of general anaesthesia on endoplasmic reticulum stress: propofolInternational journal of medical sciences · 2019
    Article
  9. Article
  10. Article
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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

6 authors at 1 institution in 1 country.

Xuezhi ZhouState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, Guangdong, China.
Yantao WeiState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, Guangdong, China.
Suo QiuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, Guangdong, China.
Yue XuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, Guangdong, China.
Ting ZhangState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, Guangdong, China.
Shaochong ZhangState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, Guangdong, China.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is the major cause of loss of sight globally. There is currently no effective treatment available. Retinal pigment epithelial (RPE) cells are an important part of the outer blood-retina barrier and their death is a determinant of AMD. Propofol, a common clinically used intravenous anesthetic agent, has been shown to act as an efficacious neuroprotective agent with antioxidative and anti-inflammatory properties in vivo and in vitro. However, little is known about its effects on RPE cells. The purpose of our research was to investigate whether propofol could protect RPE cells from apoptosis through endoplasmic reticulum (ER) stress-dependent pathways. To this end, prior to stimulation with thapsigargin (TG), ARPE-19 cells were pretreated with varying concentrations of propofol. A protective effect of propofol in TG-treated ARPE-9 was apparent, TUNEL and flow cytometric assays showed decreased apoptosis. We further demonstrated that propofol pretreatment attenuated or inhibited the effects caused by TG, such as upregulation of Bax, BiP, C/EBP homologous protein (CHOP), active caspase 12, and cleaved caspase 3, and downregulation of Bcl2. It also decreased the TG-induced levels of ER stress-related molecules such as p-PERK, p-eIF2α, and ATF4. Furthermore, it downregulated the expression of nuclear factor κB (NF-κB). This study elucidated novel propofol-induced cellular mechanisms for antiapoptotic activities in RPE cells undergoing ER stress and demonstrated the potential value of using propofol in the treatment of AMD.

Indexed as

Activating Transcription Factor 4Anesthetics, IntravenousAntioxidantsApoptosisbcl-2-Associated X ProteinCalciumCaspase 12Caspase 3Cell LineCell SurvivaleIF-2 KinaseEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEpithelial CellsEukaryotic Initiation Factor-2Gene Expression RegulationActivating Transcription Factor 4Anesthetics, IntravenousAntioxidantsATF4 protein, humanBAX protein, humanbcl-2-Associated X ProteinBCL2 protein, humanCalciumCASP12 protein, humanCASP3 protein, humanCaspase 12Caspase 3DDIT3 protein, humanEIF2AK3 protein, humaneIF-2 KinaseEndoplasmic Reticulum Chaperone BiPEukaryotic Initiation Factor-2Heat-Shock ProteinsNeuroprotective AgentsNF-kappa BPropofolProto-Oncogene Proteins c-bcl-2ThapsigarginTranscription Factor CHOP

Identifiers

PMID27311010
PMCPMC4910991
OpenAlexW2424481748

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.