Evidence map›Paper›PMID 31949884›Full record

ArticleOxidative medicine and cellular longevity2019

LncRNA MALAT1 Suppression Protects Endothelium against oxLDL-Induced Inflammation via Inhibiting Expression of MiR-181b Target Gene TOX.

Liuqing Wang, Yinliang Qi, Yi Wang, Haitao Tang, Zhenzhen Li, Yuan Wang, Songtao Tang, Huaqing Zhu

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

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  5. Long Noncoding RNA MALAT1: Salt-Sensitive Hypertension.International journal of molecular sciences · 2024
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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

8 authors at 1 institution in 1 country.

Liuqing WangDepartment of Clinical Laboratory, The Third Clinical School of Heifei of Anhui Medical University, Hefei 230051, China.
Yinliang QiGeneral Department of Hyperbaric Oxygen, Hefei Hospital Affiliated to Anhui Medical University, Hefei 230011, China.
Yi WangLaboratory of Molecular Biology and Department of Biochemistry, Anhui Medical University, Hefei 230032, China.
Haitao TangLaboratory of Molecular Biology and Department of Biochemistry, Anhui Medical University, Hefei 230032, China.
Zhenzhen LiLaboratory of Molecular Biology and Department of Biochemistry, Anhui Medical University, Hefei 230032, China.
Yuan WangLaboratory of Molecular Biology and Department of Biochemistry, Anhui Medical University, Hefei 230032, China.
Songtao TangDepartment of Endocrinology, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.ORCID https://orcid.org/0000-0002-8001-0158
Huaqing ZhuLaboratory of Molecular Biology and Department of Biochemistry, Anhui Medical University, Hefei 230032, China.ORCID https://orcid.org/0000-0002-5013-2269
Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rare studies have been conducted to investigate the exact interactions between lung adenocarcinoma transcript 1 (MALAT1), thymocyte selection-associated high mobility group box (TOX), and miRNAs in the pathogenesis of atherosclerosis (AS). We aim to investigate the crosstalk between MALAT1 and TOX and evaluate whether the regulatory mechanism was associated with the miRNA network. AS tissues were collected to determine the level of MALAT1 expression in AS patients, together with determination of miR-181b expression. Cultured endothelial cells were utilized to analyze the expressions of MALAT1, miR-181b, and TOX in the presence of oxLDL. Luciferase activity assay was conducted to evaluate the potential target sites of miR-181b on MALAT1 and TOX. In this study, we demonstrated that MALAT1 was upregulated in patients with AS. MALAT1 silencing significantly downregulated the expression of the miR-181b target gene TOX via reversing the effect of miR181b. Importantly, positive modulation of miR181b and inhibition of MALAT1 and TOX significantly attenuated oxLDL-induced endothelial inflammation and oxidative stress. Moreover, the MAPK signal pathways in endothelial cells were also inhibited through regulation of above endogenous RNAs. In summary, MALAT1 suppression protects the endothelium from oxLDL-induced inflammation and oxidative stress in endothelial cells by upregulation of miR-181b and downregulation of TOX.

Indexed as

ApoptosisAtherosclerosisCase-Control StudiesCell ProliferationCells, CulturedEndothelium, VascularFemaleGene Expression RegulationHigh Mobility Group ProteinsHumansInflammationLipoproteins, LDLMaleMicroRNAsMiddle AgedOxidative StressHigh Mobility Group ProteinsLipoproteins, LDLMALAT1 long non-coding RNA, humanMicroRNAsMIrn181 microRNA, humanoxidized low density lipoproteinProtective AgentsRNA, Long NoncodingTOX protein, human

Identifiers

PMID31949884
PMCPMC6942911
OpenAlexW2996685756

What OpenQuestion holds

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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.