Evidence map›Paper›PMID 30838022›Full record

ArticleFrontiers in genetics2019

Long Non-coding RNA MEG3 Attenuates the Angiotensin II-Induced Injury of Human Umbilical Vein Endothelial Cells by Interacting With p53.

Jingwen Song, Songqun Huang, Kaizhong Wang, Wei Li, Lizhi Pao, Feng Chen, Xianxian Zhao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2019. 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
0.9field-weighted citation impact, top 31% 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, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Genetic Deletion of theNon-coding RNA · 2023
    Article
  5. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. [Regulation of long non-coding RNA in cartilage injury of osteoarthritis].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2020
    Article
  11. Knockdown of Long Noncoding RNA (lncRNA) AK094457 Relieved Angiotensin II Induced Vascular Endothelial Cell Injury.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
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

7 authors at 2 institutions in 1 country.

Jingwen SongDepartment of Cardiovascularology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Songqun HuangDepartment of Cardiovascularology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Kaizhong WangDepartment of Cardiovascularology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Wei LiInstitute of Tumor, Second Military Medical University, Shanghai, China.
Lizhi PaoDepartment of Cardiovascularology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Feng ChenDepartment of Cardiovascularology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Xianxian ZhaoDepartment of Cardiovascularology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China.
Changhai Hospital · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin II (Ang II)-induced damage to endothelial cells (ECs) plays a crucial role in the pathogenesis of cardiovascular disease. This study aimed to investigate the role of maternally expressed gene 3 (Meg3) in endothelial cell injury. A lncRNA human gene expression microarray analysis was used to identify differentially expressed lncRNAs in human umbilical vein endothelial cell (HUVECs). Cell viability, apoptosis, and migration were then assessed Ang II-treated HUVECs. qRT-PCR and western blotting were performed to detect the expression level of p53 after Meg3 knockdown and overexpression. We observed that Ang II treatment decreased the Meg3 level in HUVECs. Next, both knockdown of Meg3 and Ang II decreased cell viability, increased apoptotic cell rate and impair migration function in HUVECs. Furthermore, overexpression of Meg3 inhibited cell apoptosis, and increased cell migration by enhancing p53 transcription on its target genes, including CRP, ICAM-1, VEGF, and HIF-1α. Our findings indicate that Meg3 might be associated with cardiovascular disease development.

Indexed as

Ang IIcardiovascular diseaseHUVECsMeg3p53

Identifiers

PMID30838022
PMCPMC6389612
OpenAlexW2916818899

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.