Evidence map›Paper›PMID 29022894›Full record

ArticleCell death & disease2017

Adiponectin controls the apoptosis and the expression of tight junction proteins in brain endothelial cells through AdipoR1 under beta amyloid toxicity.

Juhyun Song, Seong-Min Choi, Daniel J Whitcomb, Byeong C Kim

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.8field-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

36 citing papers in PubMed, 61 citations in OpenAlex.

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  10. Physiological and Pathological Remodeling of Cerebral Microvessels.International journal of molecular sciences · 2022
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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 3 institutions in 2 countries.

Juhyun SongDepartment of Biomedical Sciences, Center for Creative Biomedical Scientists at Chonnam National University, Gwangju 61469, South Korea.
Seong-Min ChoiDepartment of Neurology, Chonnam National University Medical School, Gwangju 61469, South Korea.
Daniel J WhitcombHenry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, School of Clinical Sciences, Faculty of Healthy Sciences, University of Bristol, Whitson Street, Bristol BS1 3NY, UK.
Byeong C KimDepartment of Neurology, Chonnam National University Medical School, Gwangju 61469, South Korea.
Chonnam National University Hospital · KRChonnam National University · KRUniversity of Bristol · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease, characterized by excessive beta amyloid (Aβ) deposition in brain, leading to blood-brain barrier (BBB) disruption. The mechanisms of BBB disruption in AD are still unclear, despite considerable research. The adipokine adiponectin is known to regulate various metabolic functions and reduce inflammation. Though adiponectin receptors have been reported in the brain, its role in the central nervous system has not been fully characterized. In the present study, we investigate whether adiponectin contributes to the tight junction integrity and cell death of brain endothelial cells under Aβ-induced toxicity conditions. We measured the expression of adiponectin receptors (AdipoR1 and AdipoR2) and the alteration of tight junction proteins in in vivo 5xFAD mouse brain. Moreover, we examined the production of reactive oxygen species (ROS) and the loss of tight junction proteins such as Claudin 5, ZO-1, and inflammatory signaling in in vitro brain endothelial cells (bEnd.3 cells) under Aβ toxicity. Our results showed that Acrp30 (a globular form of adiponectin) reduces the expression of proinflammatory cytokines and the expression of RAGE as Aβ transporters into brain. Moreover, we found that Acrp 30 attenuated the apoptosis and the tight junction disruption through AdipoR1-mediated NF-κB pathway in Aβ-exposed bEnd.3 cells. Thus, we suggest that adiponectin is an attractive therapeutic target for treating BBB breakdown in AD brain.

Indexed as

AdiponectinAlzheimer DiseaseAmyloid beta-PeptidesAnimalsApoptosisBlood-Brain BarrierBrainCell LineCell SurvivalClaudin-5Endothelial CellsLow Density Lipoprotein Receptor-Related Protein-1MaleMiceMice, Inbred C57BLMice, TransgenicAdiponectinadiponectin receptor 1, mouseadiponectin receptor 2, mouseAdipoq protein, mouseAger protein, mouseAmyloid beta-PeptidesClaudin-5Cldn5 protein, mouseLow Density Lipoprotein Receptor-Related Protein-1Lrp1 protein, mouseNF-kappa BNitric OxideReactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsReceptors, AdiponectinReceptors, LDLTjp1 protein, mouseTumor Suppressor ProteinsZonula Occludens-1 Protein

Identifiers

PMID29022894
PMCPMC5682657
OpenAlexW2761487449

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.