Evidence map›Paper›PMID 35320491›Full record

ArticleJournal of molecular histology2022

A novel miR-338-3p/SLC1A5 axis reprograms retinal pigment epithelium to increases its resistance to high glucose-induced cell ferroptosis.

Jing Zhou, Caoyu Sun, Xu Dong, Hui Wang

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Article in Journal of molecular histology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 38 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

4 authors at 2 institutions in 1 country.

Jing ZhouThe 4 th People's Hospital of Shenyang, Huanghe South Street No. 20, Huanggu District, 110031, Shenyang, Liaoning Province, China.
Caoyu SunThe 4 th People's Hospital of Shenyang, Huanghe South Street No. 20, Huanggu District, 110031, Shenyang, Liaoning Province, China.
Xu DongThe 4 th People's Hospital of Shenyang, Huanghe South Street No. 20, Huanggu District, 110031, Shenyang, Liaoning Province, China.
Hui WangThe 4 th People's Hospital of Shenyang, Huanghe South Street No. 20, Huanggu District, 110031, Shenyang, Liaoning Province, China. huiwanghomewh@163.com.ORCID http://orcid.org/0000-0001-6498-7009
The Sixth People's Hospital of Shenyang · CNLiaoning Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOxidative stress-induced cell ferroptosis occurs during the pathogenesis of diabetic retinopathy (DR), but the detailed molecular mechanisms are still unclear. The present study aimed to investigate this issue. MATERIALS AND

methodsThe retinal pigment epithelium (RPE) was treated with high glucose (30 mM) in vitro to mimic the realistic conditions of DR progression in vivo. Cell viability was determined by MTT assay and trypan blue staining assay. Gene expressions were examined by Real-Time qPCR and Western Blot analysis. FCM was used to detect cell apoptosis and ROS generation. Dual-luciferase reporter gene system assay was used to verify the targeting sites.

resultsHigh glucose increased reactive oxygen species (ROS) levels, promoted cell ferroptosis, and suppressed cell proliferation and viability in RPE, which were reversed by co-treating cells with both a ferroptosis inhibitor ferrostatin-1 and an ROS scavenger, N-acetyl-L-Cysteine (NAC). In addition, we screened out a miR-338-3p/ASCT2 (SLC1A5) axis that played an important role in this process. Mechanistically, miR-338-3p targeted the 3' untranslated regions (3'UTR) of SLC1A5 for its inhibition and degradation, and high glucose downregulated SLC1A5 by upregulating miR-338-3p in RPE cells. Next, the miR-338-3p inhibitor and SLC1A5 overexpression vectors were delivered into the RPE cells, and the following gain- and loss-of-function experiments validated that both miR-338-3p ablation and SLC1A5 upregulation abrogated the regulating effects of high glucose on cell proliferation, viability, ferroptosis and ROS production in RPE cells.

conclusionsCollectively, data in the present study indicated that targeting the miR-338-3p/SLC1A5 axis could block high glucose-induced ferroptosis in RPE cells.

Indexed as

Amino Acid Transport System ASCDiabetic RetinopathyFerroptosisMicroRNAsMinor Histocompatibility AntigensApoptosisCell ProliferationGlucoseHumansReactive Oxygen SpeciesRetinal Pigment EpitheliumAmino Acid Transport System ASCGlucoseMicroRNAsMinor Histocompatibility AntigensMIRN338 microRNA, humanReactive Oxygen SpeciesSLC1A5 protein, humanCell ferroptosisDiabetic retinopathymiR-338-3pROSSLC1A5

Identifiers

PMID35320491
OpenAlexW4220759295

What Socratic 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 Socratic graph.