Evidence map›Paper›PMID 30106090›Full record

ArticleInternational journal of molecular medicine2018

TREK‑TRAAK two‑pore domain potassium channels protect human retinal pigment epithelium cells from oxidative stress.

Hao Huang, Han Li, Kangpei Shi, Lei Wang, Xiaotong Zhang, Xiaobo Zhu

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Elevated expression of TREK-TRAAK KInternational journal of ophthalmology · 2019
    Article
  8. 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

6 authors at 1 institution in 1 country.

Hao HuangState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Han LiState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Kangpei ShiState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Lei WangState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Xiaotong ZhangState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Xiaobo ZhuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the current study was to explore the potential of TREK‑TRAAK two‑pore domain potassium (K2P) channels in protecting human retinal pigment epithelium (hRPE) cells against oxidative stress. hRPE cells were obtained from donors, and then cell identification and detection of the expression levels of TREK‑TRAAK K2P channels in hRPE cells were conducted. Subsequently, tert‑butyl hydroperoxide (t‑BH) was used to induce oxidative stress in hRPE cells. Docosahexaenoic acid (DHA) was used to stimulate and fluoxetine was used to inhibit the TREK‑TRAAK K2P channels. The survival rates of hRPE cells under oxidative stress were examined using flow cytometry. Apoptosis‑associated factors, including Bax, Bcl‑2, cleaved‑caspase‑3, αB‑crystallin and their mRNAs, were examined using immunofluorescence, western blot and reverse transcription‑polymerase chain reaction analyses. Variations in the cytoarchitecture were observed by immunofluorescence and electron microscopy. The cells examined in the present study were identified as hRPE cells. All members in the TREK‑TRAAK K2P channel family (including TREK‑1, TREK‑2 and TRAAK) were found to be expressed in hRPE cells. Stimulation of TREK‑TRAAK K2P channels increased the survival rates of hRPE cells under oxidative stress and the levels of intracellular protective factors, such as Bcl‑2 and αB‑crystallin. By contrast, inhibition of these channels decreased the cell survival rates and increased apoptosis enhancing factors, such as Bax and cleaved‑caspase‑3. Further examination of the cytoarchitecture revealed that TREK‑TRAAK K2P channels protected the integrity of the hRPE cell structure against oxidative stress. In conclusion, the present study suggested that the activated TREK‑TRAAK K2P channels serve a role in protecting hRPE cells against the oxidative stress induced by t‑BH, which indicated that these K2P channels are potential novel targets in retinal protection and provided a new direction for research and therapy in retinal degeneration diseases.

Indexed as

Adultalpha-Crystallinsbeta-CrystallinsBlotting, WesternDocosahexaenoic AcidsFemaleFlow CytometryFluorescent Antibody TechniqueHumansMaleOxidative StressPotassium ChannelsPotassium Channels, Tandem Pore DomainProto-Oncogene Proteins c-bcl-2Retinal Pigment Epitheliumtert-Butylhydroperoxidealpha-Crystallinsbeta-CrystallinsDocosahexaenoic AcidsKCNK4 protein, humanpotassium channel protein TREK-1Potassium ChannelsPotassium Channels, Tandem Pore DomainProto-Oncogene Proteins c-bcl-2tert-Butylhydroperoxide

Identifiers

PMID30106090
PMCPMC6192786
OpenAlexW2887812718

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.