Evidence map›Paper›PMID 29237426›Full record

ArticleBMC pulmonary medicine2017

Long non-coding RNA MALAT1 protects preterm infants with bronchopulmonary dysplasia by inhibiting cell apoptosis.

Cheng Cai, Jiajun Qiu, Gang Qiu, Yihuan Chen, Zhijun Song, Juan Li, Xiaohui Gong

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

29 citing papers in PubMed, 43 citations in OpenAlex.

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  10. LncRNAMolecules (Basel, Switzerland) · 2022
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  12. Mechanistic studies of MALAT1 in respiratory diseases.Frontiers in molecular biosciences · 2022
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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

7 authors at 2 institutions in 1 country.

Cheng CaiDepartment of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, People's Republic of China, 200062.
Jiajun QiuDepartment of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, People's Republic of China, 200062.
Gang QiuDepartment of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, People's Republic of China, 200062.
Yihuan ChenDepartment of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, People's Republic of China, 200062.
Zhijun SongDepartment of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, People's Republic of China, 200062.
Juan LiDepartment of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, People's Republic of China, 200062.
Xiaohui GongDepartment of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, People's Republic of China, 200062. gongxh@shchildren.com.cn.
Shanghai Jiao Tong University · CNShanghai Children's Hospital · CN

Funding

the National Natural Science Foundation of China 81571467
6 · The paper itself

Abstract

backgroundBronchopulmonary dysplasia (BPD) is a neonatal chronic lung disease characterized by impaired pulmonary alveolar development in preterm infants. Until now, little is known about the molecular and cellular basis of BPD. There is increasing evidence that lncRNAs regulate cell proliferation and apoptosis during lung organogenesis. The potential role of lncRNAs in the pathogenesis of BPD is unclear. This study aims to clarify the role of MALAT1 during the process of BPD in preterm infants and illustrate the protective effect of MALAT1 involved in preterm infants.

methodsWe assessed the expression of MALAT1 in BPD mice lung tissues by reanalyzing dataset GSE25286 (Mouse GEO Genome 4302 Array) from gene expression database gene expression omnibus (GEO), and verified MALAT1 expression in BPD patients by realtime q-PCR. Then the role of MALAT1 in regulating cell biology was examined by profiling dataset GSE43830. The expression of CDC6, a known antiapoptopic gene was verified in BPD patients and the alveolar epithelial cell line A549 cells in which MALAT1 was knocked down. Cell apoptosis was determined by FACS using PI/Annexin-V staining.

resultsThe expression of MALAT1 was significantly evaluated in lung tissues of BPD mice at day 14 and day 29 compared to WT (P < 0.05). In consistent with mRNA array profiling analysis, MALAT1 expression level in blood samples from preterm infants with BPD was significantly increased. Bioinformative data analysis of MALAT1 knockdown in WI-38 cells showed various differentially expressed genes were found enriched in apoptosis related pathway. Down-regulation of antiapoptopic gene, CDC6 expression was further verified by q-PCR result. PI/Annexin-V apoptisis assay results showed that MALAT1 knocked down in the alveolar epithelial cell line (A549) promotes cell apoptosis.

conclusionsIn our study, we found that up-regulation of lncRNA MALAT1 could protect preterm infants with BPD by inhibiting cell apoptosis. These data provide novel insights into MALAT1 regulation which may be relevant to cell fate and shed light on BPD prevention and treatment.

Indexed as

ApoptosisInfant, PrematureA549 CellsAnimalsAnimals, NewbornBronchopulmonary DysplasiaCell ProliferationDisease Models, AnimalGene Knockdown TechniquesHumansInfant, NewbornLungMiceOligonucleotide Array Sequence AnalysisReal-Time Polymerase Chain ReactionRNA, Long NoncodingMALAT1 long non-coding RNA, humanMalat1 long non-coding RNA, mouseRNA, Long NoncodingRNA, MessengerApoptosisBPDHyperoxiaMALAT1Preterm neonates

Identifiers

PMID29237426
PMCPMC5729463
OpenAlexW2774868668

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.