| First Author | Ke XF | Year | 2014 |
| Journal | Biochem Biophys Res Commun | Volume | 450 |
| Issue | 4 | Pages | 1297-303 |
| PubMed ID | 24996183 | Mgi Jnum | J:220141 |
| Mgi Id | MGI:5632278 | Doi | 10.1016/j.bbrc.2014.06.125 |
| Citation | Ke XF, et al. (2014) MicroRNA-203 accelerates apoptosis in LPS-stimulated alveolar epithelial cells by targeting PIK3CA. Biochem Biophys Res Commun 450(4):1297-303 |
| abstractText | 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 5d 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. |
