Evidence map›Paper›PMID 35902594›Full record

ArticleScientific reports2022

Effect of cytokine-induced alterations in extracellular matrix composition on diabetic retinopathy-relevant endothelial cell behaviors.

Meredith J Giblin, Cayla D Ontko, John S Penn

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 18 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

Meredith J GiblinDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, USA. Meredith.j.giblin@vanderbilt.edu.
Cayla D OntkoDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, USA.
John S PennDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, USA.
Vanderbilt University · USVanderbilt University Medical Center · US

Funding

Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Kevin L Schey · 1989 to 2026
$19.6M
RETINOPATHY OF PREMATURITY--UNDERSTAND ITS PATHOGENESISR01EY007533 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PENN, JOHN S. · 1993 to 2018
$7.0M
In Vivo Molecular Imaging of the RetinaR01EY023397 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PENN, JOHN S., UDDIN, MD IMAM · 2013 to 2022
$3.6M
The calcineurin/NFAT signaling axis in diabetic retinopathy pathogenesisR01EY023639 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PENN, JOHN S. · 2014 to 2017
$1.8M
Training Program in Quantitative Ocular GenomicsT32EY021453 · NEI · VANDERBILT UNIVERSITY · PI BRANTLEY, MILAM A, COX, NANCY J · 2011 to 2020
$1.4M
NEI NIH HHS P30 EY008126NEI NIH HHS R01 EY007533NEI NIH HHS R01 EY023397NEI NIH HHS R01 EY023639NEI NIH HHS T32 EY021453NIDDK NIH HHS P30 DK020593NIH HHS R01-EY07533NIH HHS T32-EY021453
6 · The paper itself

Abstract

Retinal vascular basement membrane (BM) thickening is an early structural abnormality of diabetic retinopathy (DR). Recent studies suggest that BM thickening contributes to the DR pathological cascade; however, much remains to be elucidated about the exact mechanisms by which BM thickening develops and subsequently drives other pathogenic events in DR. Therefore, we undertook a systematic analysis to understand how human retinal microvascular endothelial cells (hRMEC) and human retinal pericytes (hRP) change their expression of key extracellular matrix (ECM) constituents when treated with diabetes-relevant stimuli designed to model the three major insults of the diabetic environment: hyperglycemia, dyslipidemia, and inflammation. TNFα and IL-1β caused the most potent and consistent changes in ECM expression in both hRMEC and hRP. We also demonstrate that conditioned media from IL-1β-treated human Müller cells caused dose-dependent, significant increases in collagen IV and agrin expression in hRMEC. After narrowing our focus to inflammation-induced changes, we sought to understand how ECM deposited by hRMEC and hRP under inflammatory conditions affects the behavior of naïve hRMEC. Our data demonstrated that diabetes-relevant alterations in ECM composition alone cause both increased adhesion molecule expression by and increased peripheral blood mononuclear cell (PBMC) adhesion to naïve hRMEC. Taken together, these data demonstrate novel roles for inflammation and pericytes in driving BM pathology and suggest that inflammation-induced ECM alterations may advance other pathogenic behaviors in DR, including leukostasis.

Indexed as

Diabetes MellitusDiabetic RetinopathyCytokinesEndothelial CellsExtracellular MatrixHumansInflammationLeukocytes, MononuclearRetinaCytokines

Identifiers

PMID35902594
PMCPMC9334268
OpenAlexW4288439446

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.