Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 450, Issue 4, Pages 1297-1303Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2014.06.125
Keywords
microRNA-203; PIK3CA; Apoptosis; Lipopolysaccharide
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Funding
- Zhejiang Academy of Medical Sciences
- Zhejiang Provincial Natural Science Foundation [Y13H280002]
- Zhejiang Provincial Science and Technology Foundation [2012F30026]
- National Natural Science Foundation of China [81202977]
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The pathogenesis of endotoxin-induced acute lung injury (ALI) remains obscure and has not been well elucidated hitherto. Recently, microRNAs have distinct expression profiles in innate immunity, inflammation, and infection. However, the functions of microRNAs in ALI remain unknown. In this study, the functions of microRNAs in the development of ALI were investigated to identify potential drug targets. MicroRNA-203 (miR-203) expression in the lung tissues of lipopolysaccharide (LPS)-challenged mice was found to be significantly upregulated and peaked 5 d post-LPS injection. MiR-203 overexpression in A549 cells significantly promoted cell apoptosis by inducing S-phase cell-cycle arrest. MiR-203 overexpression also inhibited the protein expression of phosphoinositide 3-kinase catalytic subunit alpha (PIK3CA), a direct target of miR-203 identified by bioinformatics, thereby suppressing the PI3K/Akt pathway. Moreover, repressed miR-203 effectively attenuated LPS-induced interstitial pneumonia. Therefore, regulating or inhibiting miR-203 may be of therapeutic potential in pneumonia and ALI. (C) 2014 Elsevier Inc. All rights reserved.
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