ArticleInternational journal of molecular medicine2018
TREK‑TRAAK two‑pore domain potassium channels protect human retinal pigment epithelium cells from oxidative stress.
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.
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.
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.
Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- The retinal pigment epithelium displays electrical excitability and lateral signal spreading.BMC biology · 2023Article
- Negative Influence by the Force: Mechanically Induced Hyperpolarization via KInternational journal of molecular sciences · 2021Review
- Two-Pore Domain Potassium Channel in Neurological Disorders.The Journal of membrane biology · 2021Review
- PSCs Reveal PUFA-Provoked Mitochondrial Stress as a Central Node Potentiating RPE Degeneration in Bietti's Crystalline Dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Effect of 6-Shogaol on the Glucose Uptake and Survival of HT1080 Fibrosarcoma Cells.Pharmaceuticals (Basel, Switzerland) · 2019Article
- Activation of the TRAAK two-pore domain potassium channels in rd1 mice protects photoreceptor cells from apoptosis.International journal of ophthalmology · 2019Article
- Elevated expression of TREK-TRAAK KInternational journal of ophthalmology · 2019Article
- Differential Expression of BDNF and BIM in Streptozotocin-induced Diabetic Rat Retina After Fluoxetine Injection.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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
Identifiers
What OpenQuestion holds
Registered trials
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.