Evidence map›Paper›PMID 36736696›Full record

ArticleJournal of advanced research2023

LncRNA NIPA1-SO confers atherosclerotic protection by suppressing the transmembrane protein NIPA1.

Min Jiang, Yu Song, Mei-Xia Ren, Run-Chao He, Xian-Hui Dong, Xue-Heng Li, Zhi-Feng Lu, Shu Li, Jia Wu, Yan-Rou Bei and 10 more

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 14 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

20 authors at 8 institutions in 3 countries.

Min JiangDepartment of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangzhou 510620, China.
Yu SongDepartment of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangzhou 510620, China.
Mei-Xia RenShengli Clinical Medical College of Fujian Medical University, Fujian Medical University, Fuzhou 350001, China; Department of Geriatric Medicine, Fujian Provincial Hospital, Fujian Key Laboratory of Geriatrics, Fujian Provincial Center for Geriatrics, Fuzhou 350013, China.
Run-Chao HeDepartment of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangzhou 510620, China.
Xian-Hui DongDepartment of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangzhou 510620, China.
Xue-Heng LiLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Zhi-Feng LuLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Shu LiDepartment of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangzhou 510620, China.
Jia WuDepartment of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangzhou 510620, China.
Yan-Rou BeiLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Fei LiuDepartment of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangzhou 510620, China.
Yan LongDepartment of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangzhou 510620, China.
Shao-Guo WuDepartment of Clinical Laboratory, Guangzhou Twelfth People's Hospital, Guangzhou 510620, China.
Xue-Hui LiuDepartment of Clinical Laboratory, Guangzhou Twelfth People's Hospital, Guangzhou 510620, China.
Li-Mei WuDepartment of Clinical Laboratory, Guangzhou Twelfth People's Hospital, Guangzhou 510620, China.
Hong-Ling YangDepartment of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangzhou 510620, China.
David G McVeyDepartment of Cardiovascular Sciences & NIHR Leicester Biomedical Research Centre, University of Leicester, Leicester LE3 9QP, UK.
Xiao-Yan DaiKey Laboratory of Molecular Target & Clinical Pharmacology and the State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, Guangdong 511436, China. Electronic address: xdai@gzhmu.edu.cn.
Shu YeCardiovascular Translational Research Programme, National University of Singapore, Singapore; Shantou University Medical College, Shantou, China. Electronic address: sy127@leicester.ac.uk.
Yan-Wei HuDepartment of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangzhou 510620, China; Laboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. Electronic address: ywhu0618@163.com.
Guangzhou Medical University · CNGuangzhou Women and Children Medical Center · CNSouthern Medical University · CNTwelfth Guangzhou City People's Hospital · CNFujian Provincial Hospital · CNNanfang Hospital · CNShantou University Medical College · CNUniversity of Leicester · GB

Funding

British Heart Foundation PG/16/9/31995British Heart Foundation PG/18/73/34059British Heart Foundation RG/16/13/32609British Heart Foundation RG/19/9/34655
6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) are emerging as important players in gene regulation and cardiovascular diseases. However, the roles of lncRNAs in atherosclerosis are poorly understood. In the present study, we found that the levels of NIPA1-SO were decreased while those of NIPA1 were increased in human atherosclerotic plaques. Furthermore, NIPA1-SO negatively regulated NIPA1 expression in human umbilical vein endothelial cells (HUVECs). Mechanistically, NIPA1-SO interacted with the transcription factor FUBP1 and the NIPA1 gene. The effect of NIPA1-SO on NIPA1 protein levels was reversed by the knockdown of FUBP1. NIPA1-SO overexpression increased, whilst NIPA1-SO knockdown decreased BMPR2 levels; these effects were enhanced by the knockdown of NIPA1. The overexpression of NIPA1-SO reduced while NIPA1-SO knockdown increased monocyte adhesion to HUVECs; these effects were diminished by the knockdown of BMPR2. The lentivirus-mediated-overexpression of NIPA1-SO or gene-targeted knockout of NIPA1 in low-density lipoprotein receptor-deficient mice reduced monocyte-endothelium adhesion and atherosclerotic lesion formation. Collectively, these findings revealed a novel anti-atherosclerotic role for the lncRNA NIPA1-SO and highlighted its inhibitory effects on vascular inflammation and intracellular cholesterol accumulation by binding to FUBP1 and consequently repressing NIPA1 expression.

Indexed as

AtherosclerosisPlaque, AtheroscleroticRNA, Long NoncodingAnimalsDNA-Binding ProteinsHumansHuman Umbilical Vein Endothelial CellsMembrane ProteinsMiceRNA-Binding ProteinsDNA-Binding ProteinsFUBP1 protein, humanMembrane ProteinsNIPA1 protein, humanRNA-Binding ProteinsRNA, Long NoncodingAtherosclerosisLncRNANIPA1Vascular adhesion molecule

Identifiers

PMID36736696
PMCPMC10703723
OpenAlexW4319001821

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.