Evidence map›Paper›PMID 38601015›Full record

ArticleMolecular vision2024

EphB1 causes retinal damage through inflammatory pathways in the retina and retinal Müller cells.

Li Liu, Youde Jiang, Mohamed Al-Shabrawey, Xiaobai Ren, Sui Wang, Jena J Steinle

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 95% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. Article
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

6 authors at 2 institutions in 1 country.

Li LiuDepartment of Ophthalmology, Visual and Anatomical Sciences, Wayne State University School of Medicine, Detroit, MI.
Youde JiangDepartment of Ophthalmology, Visual and Anatomical Sciences, Wayne State University School of Medicine, Detroit, MI.
Mohamed Al-ShabraweyEye Research Center and Institute, Oakland University William Beaumont School of Medicine (OUWB-SOM), Oakland University, Oakland, MI.
Xiaobai RenDepartment of Ophthalmology, Mary M. and Sash A. Spencer Center for Vision Research, Byers Eye Institute, Stanford University, Stanford, CA.
Sui WangDepartment of Ophthalmology, Mary M. and Sash A. Spencer Center for Vision Research, Byers Eye Institute, Stanford University, Stanford, CA.
Jena J SteinleDepartment of Ophthalmology, Visual and Anatomical Sciences, Wayne State University School of Medicine, Detroit, MI.
Wayne State University · USStanford University · US

Funding

VISION RESEARCH--COREP30EY004068 · NEI · WAYNE STATE UNIVERSITY · PI LINDA D HAZLETT · 1985 to 2026
$13.2M
BMP2/ALKs Signaling System in Diabetic RetinopathyR01EY030054 · NEI · OAKLAND UNIVERSITY · PI Mohamed Al-Sayed Al-Shabrawey · 2020 to 2026
$2.0M
PKA and Epac1 inhibit TLR4 to protect the diabetic retinaR01EY030284 · NEI · WAYNE STATE UNIVERSITY · PI STEINLE, JENA J · 2020 to 2024
$1.7M
NEI NIH HHS P30 EY004068NEI NIH HHS R01 EY030054NEI NIH HHS R01 EY030284
6 · The paper itself

Abstract

Purpose: To examine whether increased ephrin type-B receptor 1 (EphB1) leads to inflammatory mediators in retinal Müller cells. Methods: Diabetic human and mouse retinal samples were examined for EphB1 protein levels. Rat Müller cells (rMC-1) were grown in culture and treated with EphB1 siRNA or ephrin B1-Fc to explore inflammatory mediators in cells grown in high glucose. An EphB1 overexpression adeno-associated virus (AAV) was used to increase EphB1 in Müller cells in vivo. Ischemia/reperfusion (I/R) was performed on mice treated with the EphB1 overexpression AAV to explore the actions of EphB1 on retinal neuronal changes in vivo. Results: EphB1 protein levels were increased in diabetic human and mouse retinal samples. Knockdown of EphB1 reduced inflammatory mediator levels in Müller cells grown in high glucose. Ephrin B1-Fc increased inflammatory proteins in rMC-1 cells grown in normal and high glucose. Treatment of mice with I/R caused retinal thinning and loss of cell numbers in the ganglion cell layer. This was increased in mice exposed to I/R and treated with the EphB1 overexpressing AAVs. Conclusions: EphB1 is increased in the retinas of diabetic humans and mice and in high glucose-treated Müller cells. This increase leads to inflammatory proteins. EphB1 also enhanced retinal damage in response to I/R. Taken together, inhibition of EphB1 may offer a new therapeutic option for diabetic retinopathy.

Indexed as

Diabetic RetinopathyEphrin-B1Retinal DiseasesAnimalsEpendymoglial CellsGlucoseHumansInflammation MediatorsMiceRatsRetinaEphrin-B1GlucoseInflammation Mediators

Identifiers

PMID38601015
PMCPMC11006007
OpenAlexW4394751881

What Socratic 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 Socratic graph.