Evidence map›Paper›PMID 29626212›Full record

ArticleScientific reports2018

Palmitic Acid Induces Müller Cell Inflammation that is Potentiated by Co-treatment with Glucose.

Megan E Capozzi, Meredith J Giblin, John S Penn

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. 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, 26 citations in OpenAlex.

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  12. Regulations of Retinal Inflammation: Focusing on Müller Glia.Frontiers in cell and developmental biology · 2022
    Review
  13. Article
  14. Article
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  19. Article
  20. Blocking VEGF signaling augments interleukin-8 secretionInternational journal of ophthalmology · 2020
    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

3 authors at 1 institution in 1 country.

Megan E CapozziDepartment of Molecular Physiology and Biophysics at Vanderbilt University, 1301 Medical Center Drive TVC B706-A, Nashville, TN, 37232-0028, USA. megan.e.capozzi@vanderbilt.edu.
Meredith J GiblinDepartment of Cell and Developmental Biology at Vanderbilt University, 1301 Medical Center Drive TVC B706-A, Nashville, TN, 37232-0028, USA.
John S PennDepartment of Molecular Physiology and Biophysics at Vanderbilt University, 1301 Medical Center Drive TVC B706-A, Nashville, TN, 37232-0028, USA.
Vanderbilt University Medical Center · US

Funding

The Vanderbilt Institute for Clinical and Translational Research (VICTR)UL1TR000445 · NCATS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BERNARD, GORDON RAPHAEL · 2012 to 2016
$41.4M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ALVIN C POWERS · 2012 to 2026
$29.3M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI David J. Calkins · 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
Training in Vision ResearchT32EY007135 · NEI · VANDERBILT UNIVERSITY · PI GEOFFREY F WOODMAN · 1994 to 2026
$5.8M
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
NCATS NIH HHS UL1 TR000445NEI NIH HHS P30 EY008126NEI NIH HHS R01 EY007533NEI NIH HHS R01 EY023639NEI NIH HHS T32 EY007135NEI NIH HHS T32 EY021453NIDDK NIH HHS P30 DK020593
6 · The paper itself

Abstract

Chronic hyperglycemia is thought to be the major stimulator of retinal dysfunction in diabetic retinopathy (DR). Thus, many diabetes-related systemic factors have been overlooked as inducers of DR pathology. Cell culture models of retinal cell types are frequently used to mechanistically study DR, but appropriate stimulators of DR-like factors are difficult to identify. Furthermore, elevated glucose, a gold standard for cell culture treatments, yields little to no response from many primary human retinal cells. Thus, the goal of this project was to demonstrate the effectiveness of the free fatty acid, palmitic acid and compare its use alone and in combination with elevated glucose as a stimulus for human Müller cells, a retinal glial cell type that is activated early in DR pathogenesis and uniquely responsive to fatty acids. Using RNA sequencing, we identified a variety of DR-relevant pathways, including NFκB signaling and inflammation, intracellular lipid signaling, angiogenesis, and MAPK signaling, that were stimulated by palmitic acid, while elevated glucose alone did not significantly alter any diabetes-relevant pathways. Co-treatment of high glucose with palmitic acid potentiated the expression of several DR-relevant angiogenic and inflammatory targets, including PTGS2 (COX-2) and CXCL8 (IL-8).

Indexed as

Diabetic RetinopathyDrug InteractionsEpendymoglial CellsGene Expression RegulationGlucoseHumansInflammationPalmitic AcidGlucosePalmitic Acid

Identifiers

PMID29626212
PMCPMC5889388
OpenAlexW2806990567

What OpenQuestion holds

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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.