Evidence map›Paper›PMID 30195775›Full record

ArticleMolecular therapy. Nucleic acids2018

Ribosomal Protein S3 Gene Silencing Protects Against Cigarette Smoke-Induced Acute Lung Injury.

Jinrui Dong, Wupeng Liao, Hong Yong Peh, W S Daniel Tan, Shuo Zhou, W S Fred Wong

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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  12. Inhaled RNA Therapy: From Promise to Reality.Trends in pharmacological sciences · 2020
    Review
  13. Article
  14. RNAi therapeutic strategies for acute respiratory distress syndrome.Translational research : the journal of laboratory and clinical medicine · 2019
    Review
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

6 authors at 2 institutions in 1 country.

Jinrui DongDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University Health System, Singapore, Singapore.
Wupeng LiaoDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University Health System, Singapore, Singapore.
Hong Yong PehDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University Health System, Singapore, Singapore.
W S Daniel TanDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University Health System, Singapore, Singapore.
Shuo ZhouDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University Health System, Singapore, Singapore.
W S Fred WongDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University Health System, Singapore, Singapore; Immunology Program, Life Science Institute, National University of Singapore, Singapore, Singapore; Singapore-HUJ Alliance for Research and Enterprise, Molecular Mechanisms of Inflammatory Diseases Interdisciplinary Research Group, Singapore, Singapore. Electronic address: phcwongf@nus.edu.sg.
National University Health System · SGSingapore-HUJ Alliance for Research and Enterprise · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is estimated to be the third leading cause of death by 2030. Transcription factor NF-κB may play a critical role in COPD pathogenesis. Ribosomal protein S3 (RPS3), a 40S ribosomal protein essential for executing protein translation, has recently been found to interact with the NF-κB p65 subunit and promote p65 DNA-binding activity. We sought to study whether RPS3 gene silencing could protect against cigarette-smoke (CS)-induced acute lung injury in a mouse model. Effects of an intratracheal RPS3 siRNA in CS-induced lung injury were determined by measuring bronchoalveolar lavage (BAL) fluid cell counts, levels of inflammatory and oxidative damage markers, and NF-κB translocation. Lung RPS3 level was found to be upregulated for the first time with CS exposure, and RPS3 siRNA blocked CS-induced neutrophil counts in BAL fluid. RPS3 siRNA suppressed CS-induced lung inflammatory mediator and oxidative damage marker levels, as well as nuclear p65 accumulation and transcriptional activation. RPS3 siRNA was able to disrupt CS extract (CSE)-induced NF-κB activation in an NF-κB reporter gene assay. We report for the first time that RPS3 gene silencing ameliorated CS-induced acute lung injury, probably via interruption of the NF-κB activity, postulating that RPS3 is a novel therapeutic target for COPD.

Indexed as

chronic obstructive pulmonary diseasecigarette smokeNF-KBribosomal protein S3siRNA

Identifiers

PMID30195775
PMCPMC6031153
OpenAlexW2809838522

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.