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Title: Ribosomal Protein S3 Gene Silencing Protects Against Cigarette Smoke-Induced Acute Lung Injury
Authors: Dong J. 
Liao W. 
Peh H.Y. 
Tan W.S.D. 
Zhou S.
Wong W.S.F. 
Keywords: chronic obstructive pulmonary disease; cigarette smoke; NF-KB; ribosomal protein S3; siRNA
Issue Date: 2018
Publisher: Cell Press
Citation: Dong J., Liao W., Peh H.Y., Tan W.S.D., Zhou S., Wong W.S.F. (2018). Ribosomal Protein S3 Gene Silencing Protects Against Cigarette Smoke-Induced Acute Lung Injury. Molecular Therapy - Nucleic Acids 12 : 370-380. ScholarBank@NUS Repository.
Abstract: Chronic obstructive pulmonary disease (COPD) is estimated to be the third leading cause of death by 2030. Transcription factor NF-?B 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-?B 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-?B 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-?B activation in an NF-?B 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-?B activity, postulating that RPS3 is a novel therapeutic target for COPD. © 2018 The Authors
Source Title: Molecular Therapy - Nucleic Acids
ISSN: 21622531
DOI: 10.1016/j.omtn.2018.05.027
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