Evidence map›Paper›PMID 26431165›Full record

ArticleOncotarget2015

RAGE mediated intracellular Aβ uptake contributes to the breakdown of tight junction in retinal pigment epithelium.

Sung Wook Park, Jin Hyoung Kim, Sang Min Park, Minho Moon, Ki Hwang Lee, Kyu Hyung Park, Woo Jin Park, Jeong Hun Kim

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. 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
3.0field-weighted citation impact, top 9% 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.

  1. Review
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  9. Review
  10. Oligomeric AβCells · 2021
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  13. Article
  14. Observational
  15. Article
  16. Review
  17. The Association Between Variants of Receptor for Advanced Glycation End Products (RAGE) Gene Polymorphisms and Age-Related Macular Degeneration.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  18. 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

8 authors at 5 institutions in 1 country.

Sung Wook ParkFight Against Angiogenesis-Related Blindness Laboratory, Biomedical Research Institute, Seoul National University Hospital, Jongno-gu, Seoul, Korea.
Jin Hyoung KimFight Against Angiogenesis-Related Blindness Laboratory, Biomedical Research Institute, Seoul National University Hospital, Jongno-gu, Seoul, Korea.
Sang Min ParkDepartment of Life Sciences, Life Sciences Concentration GIST (Gwangju Institute of Science and Technology), Cheomdan-gwagiro, Buk-gu, Gwangju, Korea.
Minho MoonDepartment of Biochemistry, College of Medicine, Konyang University, Seo-gu, Daejeon, Korea.
Ki Hwang LeeDepartment of Ophthalmology, Ajou University School of Medicine, Yeongtong-gu, Suwon-si, Gyeonggi-do, Korea.
Kyu Hyung ParkDepartment of Ophthalmology, College of Medicine, Seoul National University, Daehak-ro, Jongno-gu, Seoul, Korea.
Woo Jin ParkDepartment of Life Sciences, Life Sciences Concentration GIST (Gwangju Institute of Science and Technology), Cheomdan-gwagiro, Buk-gu, Gwangju, Korea.
Jeong Hun KimFight Against Angiogenesis-Related Blindness Laboratory, Biomedical Research Institute, Seoul National University Hospital, Jongno-gu, Seoul, Korea.
Seoul National University · KRSeoul National University Hospital · KRAjou University · KRGwangju Institute of Science and Technology · KRKonyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intracellular amyloid beta (Aβ) has been implicated in neuronal cell death in Alzheimer's disease (AD). Intracellular Aβ also contributes to tight junction breakdown of retinal pigment epithelium (RPE) in age-related macular degeneration (AMD). Although Aβ is predominantly secreted from neuronal cells, the mechanism of Aβ transport into RPE remains to be fully elucidated. In this study, we demonstrated that intracellular Aβ was found concomitantly with the breakdown of tight junction in RPE after subretinal injection of Aβ into the mouse eye. We also presented evidence that receptor for advanced glycation end products (RAGE) contributed to endocytosis of Aβ in RPE. siRNA-mediated knockdown of RAGE prevented intracellular Aβ accumulation as well as subsequent tight junction breakdown in RPE. In addition, we found that RAGE-mediated p38 MAPK signaling contributed to endocytosis of Aβ. Blockade of RAGE/p38 MAPK signaling inhibited Aβ endocytosis, thereby preventing tight junction breakdown in RPE. These results implicate that intracellular Aβ contributes to the breakdown of tight junction in RPE via the RAGE/p38 MAPK-mediated endocytosis. Thus, we suggest that RAGE could be a potential therapeutic target for intracellular Aβ induced outer BRB breakdown in AMD.

Indexed as

Amyloid beta-PeptidesAnimalsCells, CulturedHumansMacular DegenerationMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLReceptor for Advanced Glycation End ProductsRetinal Pigment EpitheliumSignal TransductionTight JunctionsAmyloid beta-PeptidesReceptor for Advanced Glycation End Productsage-related macular degenerationamyloid βendocytosisGerotargetreceptor for advanced glycation end productstight junction

Identifiers

PMID26431165
PMCPMC4742103
OpenAlexW2147376190

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.