Evidence map›Paper›PMID 34239033›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2021

lncRNA NEAT1 aggravates sepsis-induced lung injury by regulating the miR-27a/PTEN axis.

Xia Lv, Xiang-Yan Zhang, Qian Zhang, Ying-Jie Nie, Guang-Heng Luo, Xia Fan, Song Yang, Qing-Hua Zhao, Jian-Quan Li

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 27 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

9 authors at 2 institutions in 1 country.

Xia Lv *Emergency Intensive Care Unit, Guizhou Provincial People's Hospital, Guiyang, P. R. China.
Xiang-Yan Zhang *NHC Key Laboratory of Pulmonary Immune-related Diseases, Guizhou Provincial People's Hospital GZU, Guiyang, P. R. China.
Qian ZhangDepartment of Emergency, Guizhou Provincial People's Hospital, Guiyang, P. R. China.
Ying-Jie NieNHC Key Laboratory of Pulmonary Immune-related Diseases, Guizhou Provincial People's Hospital GZU, Guiyang, P. R. China.
Guang-Heng LuoDepartment of Urinary Surgery, Guizhou Provincial People's Hospital, Guiyang, P. R. China.
Xia FanDepartment of Pediatric Surgery, Guizhou Provincial People's Hospital, Guiyang, P. R. China.
Song YangDepartment of Endoscope, Guizhou Provincial People's Hospital, Guiyang, P. R. China.
Qing-Hua ZhaoDepartment of Nursing, The First Affiliated Hospital of Chongqing Medical University, Chongqing, P. R. China. qinghuazhaozqh0053@163.com.
Jian-Quan LiNHC Key Laboratory of Pulmonary Immune-related Diseases, Guizhou Provincial People's Hospital GZU, Guiyang, P. R. China. 401131098@qq.com.ORCID 0000-0003-3443-5136
Guizhou Provincial People's Hospital · CNThe Affiliated Yongchuan Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is an acute inflammatory reaction and a cause of acute respiratory distress syndrome (ARDS). In the present study, we explored the roles and underlying mechanism of the lncRNA Nuclear enriched abundant transcript 1 (NEAT1) in ARDS. The expression levels of genes, proteins and pro-inflammatory cytokines in patients with ARDS, LPS-stimulated cells and septic mouse models were quantified using qPCR, western blotting and ELISA assays, respectively. The molecular targeting relationship was validated by conducting a dual-luciferase reporter assay. Cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8) assay. The cell cycle phase was determined by flow cytometry assay. The expression levels of NEAT1 and pro-inflammatory cytokines were higher in patients with ARDS and septic models than in controls. Knockdown of NEAT1 significantly increased cell proliferation and cycle progression and prolonged mouse survival in vitro and in vivo. Mechanistically, miR-27a was identified as a downstream target of NEAT1 and directly inhibited PTEN expression. Further rescue experiments revealed that inhibition of miR-27a impeded the promoting effects of NEAT1 silence on cell proliferation and cycle progression, whereas inhibition of PTEN markedly weakened the inhibitory effects of NEAT1 overexpression on cell proliferation and cycle progression. Altogether, our study revealed that NEAT1 plays a promoting role in the progression of ARDS via the NEAT1/miR-27a/PTEN regulatory network, providing new insight into the pathologic mechanism behind ARDS.

Indexed as

RNA, Long NoncodingAdultAnimalsCell LineDisease Models, AnimalGene Knockdown TechniquesHumansMaleMiceMice, Inbred C57BLMicroRNAsPTEN PhosphohydrolaseRespiratory Distress SyndromeSepsisSignal TransductionMicroRNAsMIRN27 microRNA, humanMirn27 microRNA, mouseNEAT1 long non-coding RNA, humanNEAT1 long non-coding RNA, mousePTEN PhosphohydrolasePTEN protein, humanPten protein, mouseRNA, Long Noncoding

Identifiers

PMID34239033
OpenAlexW3182911978

What OpenQuestion holds

Textmetadata
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.