Evidence map›Paper›PMID 31346222›Full record

ArticleScientific reports2019

GRP78 translocation to the cell surface and O-GlcNAcylation of VE-Cadherin contribute to ER stress-mediated endothelial permeability.

Raji Lenin, Peter G Nagy, Kumar Abhiram Jha, Rajashekhar Gangaraju

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  12. The Functions of SARS-CoV-2 Receptors in Diabetes-Related Severe COVID-19.International journal of molecular sciences · 2024
    Review
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  18. Parasitology · 2023
    Article
  19. Tauroursodeoxycholic Acid Alleviates Endoplasmic Reticulum Stress-Mediated Visual Deficits in Diabetic tie2-TNF Transgenic Mice via TGR5 Signaling.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2023
    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.

Raji LeninDepartment of Ophthalmology, University of Tennessee Health Science Center, Memphis, TN, USA.
Peter G NagyDepartment of Ophthalmology, University of Tennessee Health Science Center, Memphis, TN, USA.
Kumar Abhiram JhaDepartment of Ophthalmology, University of Tennessee Health Science Center, Memphis, TN, USA.
Rajashekhar GangarajuDepartment of Ophthalmology, University of Tennessee Health Science Center, Memphis, TN, USA. sgangara@uthsc.edu.ORCID http://orcid.org/0000-0002-6664-8286
University of Tennessee Health Science Center · US

Funding

Vascular and Neuronal Repair with Adipose Stromal Cells in RetinopathyR01EY023427 · NEI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI GANGARAJU, RAJASHEKHAR · 2013 to 2017
$1.8M
NEI NIH HHS R01 EY023427
6 · The paper itself

Abstract

Increased O-GlcNAcylation, a well-known post-translational modification of proteins causally linked to various detrimental cellular functions in pathological conditions including diabetic retinopathy (DR). Previously we have shown that endothelial activation induced by inflammation and hyperglycemia results in the endoplasmic reticulum (ER) stress-mediated intercellular junction alterations accompanied by visual deficits in a tie2-TNF-α transgenic mouse model. In this study, we tested the hypothesis that increased ER stress via O-GlcNAcylation of VE-Cadherin likely contribute to endothelial permeability. We show that ER stress leads to GRP78 translocation to the plasma membrane, increased O-GlcNAcylation of proteins, particularly VE-Cadherin resulting in a defective complex partnering leading to the loss of retinal endothelial barrier integrity and increased transendothelial migration of monocytes. We further show an association of GRP78 with the VE-Cadherin under these conditions. Interestingly, cells exposed to ER stress inhibitor, tauroursodeoxycholic acid partially mitigated all these effects. Our findings suggest an essential role for ER stress and O-GlcNAcylation in altering the endothelial barrier function and reveal a potential therapeutic target in the treatment of DR.

Indexed as

Capillary PermeabilityEndoplasmic Reticulum StressAntigens, CDBlood-Retinal BarrierCadherin 5CadherinsCell MembraneCell MovementCells, CulturedEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPEndothelial CellsGlycosylationHeat-Shock ProteinsHumansMonocytesAntigens, CDCadherin 5CadherinsEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHSPA5 protein, humanHspa5 protein, mouseTaurochenodeoxycholic Acidursodoxicoltaurine

Identifiers

PMID31346222
PMCPMC6658495
OpenAlexW2963317085

What Socratic 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 Socratic graph.