Evidence map›Paper›PMID 32979189›Full record

ArticleJournal of endocrinological investigation2021

Bone marrow mesenchymal stem cells-induced exosomal microRNA-486-3p protects against diabetic retinopathy through TLR4/NF-κB axis repression.

W Li, L Jin, Y Cui, A Nie, N Xie, G Liang

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of endocrinological investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 104 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

6 authors at 2 institutions in 1 country.

W LiDepartment of Ophthalmology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, 1017 Dongmen North Road, Luohu District, Shenzhen, 518000, Guangdong, China.
L JinDepartment of Ophthalmology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, 1017 Dongmen North Road, Luohu District, Shenzhen, 518000, Guangdong, China.
Y CuiDepartment of Ophthalmology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, 1017 Dongmen North Road, Luohu District, Shenzhen, 518000, Guangdong, China.
A NieDepartment of Ophthalmology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, 1017 Dongmen North Road, Luohu District, Shenzhen, 518000, Guangdong, China.
N XieDepartment of Ophthalmology, The Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, 1017 Dongmen North Road, Luohu District, Shenzhen, 518000, Guangdong, China. Xiening88ning@163.com.
G LiangDepartment of Ophthalmology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, 53300, Guangxi, China. lianggaohua1997@163.com.
Jinan University · CNAffiliated Hospital of Youjiang Medical University for Nationalities · CN

Funding

Medical Science and Technology Research fund project of Guangdong Province B2018139
6 · The paper itself

Abstract

aimDiabetic retinopathy (DR) is a chronic disease causing health and economic burdens on individuals and society. Thus, this study is conducted to figure out the mechanisms of bone marrow mesenchymal stem cells (BMSCs)-induced exosomal microRNA-486-3p (miR-486-3p) in DR.

methodsThe putative miR-486-3p binding sites to 3'untranslated region of Toll-like receptor 4 (TLR4) was verified by luciferase reporter assay. High glucose (HG)-treated Muller cells were transfected with miR-486-3p or TLR4-related oligonucleotides and plasmids to explore theirs functions in DR. Additionally, HG-treated Muller cells were co-cultured with BMSC-derived exosomes, exosomes collected from BMSCs that had been transfected with miR-486-3p or TLR4-related oligonucleotides and plasmids to explore their functions in DR. MiR-486-3p, TLR4 and nuclear factor-kappaB (NF-κB) expression, angiogenesis-related factors, oxidative stress factors, viability and apoptosis in HG-treated Muller cells were detected by RT-qPCR, western blot analysis, ELISA, MTT assay and flow cytometry, respectively.

resultsMiR-486-3p was poorly expressed while TLR4 and NF-κB were highly expressed in HG-treated Muller cells. TLR4 was a target of miR-486-3p. Upregulating miR-486-3p or down-regulating TLR4 inhibited oxidative stress, inflammation and apoptosis, and promoted proliferation of HG-treated Muller cells. Meanwhile, BMSC-derived exosomes inhibited oxidative stress, inflammation and apoptosis, and promoted proliferation of HG-treated Muller cells. Restoring miR-486-3p further enhanced, while up-regulating TLR4 reversed, the improvement of exosomes treatment.

conclusionOur study highlights that up-regulation of miR-486-3p induced by BMSC-derived exosomes played a protective role in DR mice via TLR4/NF-κB axis repression.

Indexed as

AnimalsApoptosisCell ProliferationDiabetic RetinopathyEpendymoglial CellsExosomesGlucoseInflammationMesenchymal Stem CellsMiceMicroRNAsNF-kappa BOxidative StressProtective FactorsSignal TransductionToll-Like Receptor 4GlucoseMicroRNAsMIRN486 microRNA, mouseNF-kappa BTlr4 protein, mouseToll-Like Receptor 4Bone marrow mesenchymal stem cellsDiabetic retinopathyExosomesMicroRNA-486-3pNF-κb signaling pathwayToll-like receptor 4

Identifiers

PMID32979189
OpenAlexW3088589533

What OpenQuestion holds

Textmetadata
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.