Evidence map›Paper›PMID 27582624›Full record

ArticleMolecular vision2016

Substance P promotes the recovery of oxidative stress-damaged retinal pigmented epithelial cells by modulating Akt/GSK-3β signaling.

Sang-Min Baek, Seung-Young Yu, Youngsook Son, Hyun Sook Hong

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

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  16. Neuroprotective Peptides in Retinal Disease.Journal of clinical medicine · 2019
    Review
  17. Evidence-based complementary and alternative medicine : eCAM · 2019
    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

4 authors at 1 institution in 1 country.

Sang-Min BaekDepartment of Medicine, Graduate School, Kyung Hee University, Kyungheedae-ro, Dongdaemun-gu, Seoul, Republic of Korea.
Seung-Young YuDepartment of Ophthalmology, Kyung Hee University Hospital, Kyungheedae-ro, Dongdaemun-gu, Seoul, Republic of Korea.
Youngsook SonGraduate School of Biotechnology & Department of Genetic Engineering, College of Life Science, Kyung Hee University Global Campus, Seochun-dong, Kiheung-ku, Yong In, Republic of Korea.
Hyun Sook HongCollege of Medicine/East-West Medical Research Institute, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul, Republic of Korea.
Kyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeSenescence of the retina causes an accumulation of reactive oxygen species (ROS). Oxidative stress associated with ROS can damage RPE cells, leading to neovascularization and severe ocular disorders, including age-related macular degeneration (AMD). Thus, the early treatment of the damage caused by oxidative stress is critical for preventing the development of ocular diseases such as AMD. In this study, we examined the role of substance P (SP) in the recovery of RPE cells damaged by oxidative stress.

methodsTo induce oxidative stress, RPE cells were treated with H2O2 at various doses. Recovery from oxidative stress was studied following treatment with SP by analyzing cell viability, cell proliferation, cell apoptosis, and Akt/glycogen synthase kinase (GSK)-3β activation in RPE cells in vitro.

resultsH2O2 treatment reduced cellular viability in a dose-dependent manner. SP inhibited the reduction of cell viability due to H2O2 and caused increased cell proliferation and decreased cell apoptosis. Cell survival under oxidative stress requires the activation of Akt signaling that enables cells to resist oxidative stress-induced damage. SP treatment activated Akt/GSK-3β signaling in RPE cells, which were damaged due to oxidative stress, and the inhibition of Akt signaling in SP-treated RPE cells prevented SP-induced recovery. Pretreatment with the neurokinin 1 receptor (NK1R) antagonist reduced the recovery effect of SP on damaged RPE cells.

conclusionsSP can protect RPE cells from oxidant-induced cell death by activating Akt/GSK-3β signaling via NK1R. This study suggests the possibility of SP as a treatment for oxidative stress-related diseases.

Indexed as

ApoptosisBlotting, WesternCell LineCell ProliferationCell SurvivalEnzyme-Linked Immunosorbent AssayGlycogen Synthase Kinase 3 betaHumansHydrogen PeroxideIn Situ Nick-End LabelingNeurokinin-1 Receptor AntagonistsOxidantsOxidative StressProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptors, Neurokinin-1Glycogen Synthase Kinase 3 betaHydrogen PeroxideNeurokinin-1 Receptor AntagonistsOxidantsProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptors, Neurokinin-1Substance P

Identifiers

PMID27582624
PMCPMC4982481
OpenAlexW2507787046

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.