Evidence map›Paper›PMID 27765761›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016

Nur77 attenuates endothelin-1 expression via downregulation of NF-κB and p38 MAPK in A549 cells and in an ARDS rat model.

Yujie Jiang, Yi Zeng, Xia Huang, Yueqiu Qin, Weigui Luo, Shulin Xiang, Suren R Sooranna, Liao Pinhu

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

31 citing papers in PubMed, 52 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

8 authors at 4 institutions in 2 countries.

Yujie JiangThe First Clinical Medical College of Jinan University, Guangzhou, Guangdong Province, China.
Yi ZengDepartment of Central Laboratory, Youjiang Medical University for Nationalities, Baise, Guangxi, China.
Xia HuangThe First Clinical Medical College of Jinan University, Guangzhou, Guangdong Province, China.
Yueqiu QinDepartment of Digestive, Youjiang Medical University for Nationalities, Baise, Guangxi, China; Youjiang Medical University for Nationalities, Baise, Guangxi, China.
Weigui LuoDepartment of Respiratory Medicine.
Shulin XiangDepartment of Intensive Care Unit, the People's Hospital of Guangxi, Nanning, Guangxi, China.
Suren R SoorannaDepartment of Surgery and Cancer, Imperial College London, Chelsea and Westminster Hospital, London, United Kingdon; and.
Liao PinhuDepartment of Intensive Care Medicine, Youjiang Medical University for Nationalities, Baise, Guangxi, China liaopinhu@163.com.
Affiliated Hospital of Youjiang Medical University for Nationalities · CNJinan University · CNChelsea and Westminster Hospital · GBThe People's Hospital of Guangxi Zhuang Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute respiratory distress syndrome (ARDS) is characterized by inflammatory injury to the alveolar and capillary barriers that results in impaired gas exchange and severe acute respiratory failure. Nuclear orphan receptor Nur77 has emerged as a regulator of gene expression in inflammation, and its role in the pathogenesis of ARDS is not clear. The objective of this study is to investigate the potential role of Nur77 and its underlying mechanism in the regulation of endothelin-1 (ET-1) expression in lipopolysaccharide (LPS)-induced A549 cells and an ARDS rat model. We demonstrate that LPS induced Nur77 expression and nuclear export in A549 cells. Overexpression of Nur77 markedly decreased basal and LPS-induced ET-1 expression in A549 cells, whereas knockdown of Nur77 increased the ET-1 expression. LPS-induced phosphorylation and nuclear translocation of NF-κB and p38 MAPK were blocked by Nur77 overexpression and augmented by Nur77 knockdown in A549 cells. In vivo, LPS induced Nur77 expression in lung in ARDS rats. Pharmacological activation of Nur77 by cytosporone B (CsnB) inhibited ET-1 expression in ARDS rats, decreased LPS-induced phosphorylation of NF-κB and p38 MAPK, and relieved lung, liver, and kidney injury. Pharmacological deactivation of Nur77 by 1,1-bis-(3'-indolyl)-1-(p-hydroxyphenyl)methane (DIM-C-pPhOH, C-DIM8) had no effect on ET-1 expression and lung injury. These results indicated that Nur77 decreases ET-1 expression by suppressing NF-κB and p38 MAPK in LPS-stimulated A549 cells in vitro, and, in an LPS-induced ARDS rat model, CsnB reduced ET-1 expression and lung injury in ARDS rats.

Indexed as

Down-RegulationA549 CellsActive Transport, Cell NucleusAnimalsCell NucleusDisease Models, AnimalEndothelin-1KidneyLipopolysaccharidesLiverLungMaleNF-kappa BNuclear Receptor Subfamily 4, Group A, Member 1p38 Mitogen-Activated Protein KinasesPhenylacetatescytosporone BEndothelin-1LipopolysaccharidesNF-kappa BNR4A1 protein, humanNr4a1 protein, ratNuclear Receptor Subfamily 4, Group A, Member 1p38 Mitogen-Activated Protein KinasesPhenylacetatesRNA, Messengeracute respiratory distress syndromenuclear factor-κBp38 mitogen-activated protein kinase

Identifiers

PMID27765761
PMCPMC5206403
OpenAlexW2528853165

What OpenQuestion holds

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LicenceCC BY
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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.