Evidence map›Paper›PMID 39227412›Full record

ArticleInternational ophthalmology2024

Silencing the long noncoding RNA MALAT1 inhibits vitreous-induced epithelial-mesenchymal transition in RPE cells by regulating the PDGFRs/AKT axis.

Gukun Yang, Yikeng Huang, Duo Li, Jisen Tang, Weihong Li, Xionggao Huang

Abstract read
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In one paragraph

Article in International ophthalmology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

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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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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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.

Gukun YangDepartment of Ophthalmology, The First Affiliated Hospital of Hainan Medical University, Haikou, 571101, Hainan, People's Republic of China.
Yikeng HuangDepartment of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, People's Republic of China.
Duo LiDepartment of Ophthalmology, The First Affiliated Hospital of Hainan Medical University, Haikou, 571101, Hainan, People's Republic of China.
Jisen TangDepartment of Ophthalmology, The First Affiliated Hospital of Hainan Medical University, Haikou, 571101, Hainan, People's Republic of China.
Weihong LiDepartment of Ophthalmology, The First Affiliated Hospital of Hainan Medical University, Haikou, 571101, Hainan, People's Republic of China.
Xionggao HuangDepartment of Ophthalmology, The First Affiliated Hospital of Hainan Medical University, Haikou, 571101, Hainan, People's Republic of China. hxg_eye@163.com.

Funding

National Natural Science Foundation of China 82160199Natural Science Foundation of Hainan Province 821RC1126
6 · The paper itself

Abstract

purposeEpithelial-mesenchymal transition (EMT) is a crucial pathological process that contributes to proliferative vitreoretinopathy (PVR), and research indicates that factors present in the vitreous that target cells play pivotal roles in regulating EMT. Experimental studies have confirmed that rabbit vitreous (RV) promotes EMT in human retinal pigment epithelial (RPE) cells. The long noncoding RNA (lncRNA) MALAT1 has been implicated in EMT in various diseases. Thus, this study aimed to investigate the involvement of lncRNA MALAT1 in vitreous-induced EMT in RPE cells.

methodsMALAT1 was knocked down in ARPE-19 cells by short hairpin RNA (shRNA) transfection. Reverse transcription PCR (RT‒PCR) was used to evaluate MALAT1 expression, and Western blotting analysis was used to measure the expression of EMT-related proteins. Wound-healing, Transwell, and cell contraction assays were conducted to assess cell migration, invasion, and contraction, respectively. Additionally, cell proliferation was assessed using the CCK-8 assay, and cytoskeletal changes were examined by immunofluorescence.

resultsMALAT1 expression was significantly increased in ARPE-19 cells cultured with RV. Silencing MALAT1 effectively suppressed EMT and downregulated the associated factors snail1 and E-cadherin. Furthermore, silencing MALAT1 inhibited the RV-induced migration, invasion, proliferation, and contraction of ARPE-19 cells. Silencing MALAT1 also decreased RV-induced AKT and P53 phosphorylation.

conclusionsIn conclusion, lncRNA MALAT1 participates in regulating vitreous-induced EMT in human RPE cells; these results provide new insight into the pathogenesis of PVR and offer a potential direction for the development of antiproliferative drugs.

Indexed as

Cell MovementCell ProliferationEpithelial-Mesenchymal TransitionProto-Oncogene Proteins c-aktRetinal Pigment EpitheliumRNA, Long NoncodingAnimalsBlotting, WesternCells, CulturedGene Expression RegulationHumansRabbitsSignal TransductionVitreoretinopathy, ProliferativeVitreous BodyMALAT1 long non-coding RNA, humanProto-Oncogene Proteins c-aktRNA, Long NoncodingEpithelial-mesenchymal transitionLncRNA-MALAT1Platelet-derived growth factor receptorRetinal pigment epithelialVitreous

Identifiers

PMID39227412

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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.