Evidence map›Paper›PMID 28433754›Full record

ArticleVision research2017

miR-146a suppresses STAT3/VEGF pathways and reduces apoptosis through IL-6 signaling in primary human retinal microvascular endothelial cells in high glucose conditions.

Eun-Ah Ye, Jena J Steinle

Open access · greenAbstract read
In one paragraph

Article in Vision research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

48 citing papers in PubMed, 68 citations in OpenAlex.

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  11. Tofacitinib Regulates Endostatin via Effects on CD147 and Cathepsin S.International journal of molecular sciences · 2024
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  16. Human retinal endothelial cells express functional interleukin-6 receptor.Journal of ophthalmic inflammation and infection · 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

2 authors at 1 institution in 1 country.

Eun-Ah YeDepartment of Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, MI, United States.
Jena J SteinleDepartment of Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, MI, United States; Ophthalmology, Wayne State University School of Medicine, Detroit, MI, United States. Electronic address: jsteinle@med.wayne.edu.
Wayne State University · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
VISION RESEARCH--COREP30EY004068 · NEI · WAYNE STATE UNIVERSITY · PI LINDA D HAZLETT · 1985 to 2026
$13.2M
Mechanisms of TNFalpha-Induced Insulin Resistance in Retinal CellsR01EY022330 · NEI · WAYNE STATE UNIVERSITY · PI STEINLE, JENA J · 2013 to 2017
$1.5M
NEI NIH HHS P30 EY004068NEI NIH HHS R01 EY022330NIDDK NIH HHS P30 DK020572
6 · The paper itself

Abstract

microRNA (miRNA) play critical roles in the pathological processes of diabetic retinopathy, including inflammatory responses, insulin signaling, and angiogenesis. In addition to their regulatory functions on gene expression, miRNA is considered as a potential therapeutic target, as well as a diagnostic marker for many diseases. Our understanding on the pathological mechanisms underlying diabetic retinopathy is still incomplete and additional investigations are required to develop novel therapeutic strategies. The aim of this study was to investigate our hypothesis that miR-146a plays a role in suppressing pro-inflammatory pathways, involving STAT3 and VEGF, through regulating IL-6 signaling to reduce apoptosis of human retinal endothelial cells (REC) in high glucose conditions. Human REC were cultured in normal (5mM) glucose or high glucose medium (25mM) for 3days. We performed transfections on REC with miRNA mimics (hsa-miR-146a-5p). Overexpression of miR-146a reduced IL-6 levels, STAT3 phosphorylation, and VEGF levels in REC cultured in high glucose. Cellular apoptosis was decreased in REC overexpressing miR-146a, as demonstrated by the inhibition of DNA fragmentation. More importantly, we demonstrated that the regulatory role of miR-146a on STAT3/VEGF and apoptosis was mediated by IL-6 receptor signaling in REC. Overall, we report that miR-146a suppressed IL-6 signaling, leading to reduced levels of STAT3 and VEGF in REC in high glucose conditions, leading to decreased apoptosis. The outcome suggests that miR-146a is a potential molecular target for inhibiting inflammation and apoptosis in the diabetic retina through the suppression of the IL-6-mediated STAT3/VEGF pathway.

Indexed as

ApoptosisBlotting, WesternCells, CulturedEndothelium, VascularEnzyme-Linked Immunosorbent AssayGlucoseHumansHyperglycemiaInterleukin-6MicroRNAsPhosphorylationReal-Time Polymerase Chain ReactionRetinal VesselsRNA, Small InterferingSignal TransductionSTAT3 Transcription FactorGlucoseIL6 protein, humanInterleukin-6MicroRNAsMIRN146 microRNA, humanRNA, Small InterferingSTAT3 protein, humanSTAT3 Transcription FactorVascular Endothelial Growth Factor AVEGFA protein, humanIL-6miR-146aRECSTAT3VEGF

Identifiers

PMID28433754
PMCPMC5693785
OpenAlexW2609265540

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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.