{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T11:09:21Z","timestamp":1770980961683,"version":"3.50.1"},"reference-count":38,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2019,12,25]],"date-time":"2019-12-25T00:00:00Z","timestamp":1577232000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Gene Medicine"],"published-print":{"date-parts":[[2020,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>We aimed to investigate the biological effect of miR\u2010497 in cigarette smoke extract (CSE)\u2010damaged human bronchial epithelial (HBE) cells and the underlying molecular mechanism.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>MiR\u2010497 mimic was transfected into HBE cells to up\u2010regulate miR\u2010497 expression. Cigarette smoke extract (CSE, 20\u00a0\u03bcg\/mL) was utilized to treat HBE cells to form the injury model. Cell proliferation and apoptosis were detected by CCK8 and flow cytometry assays. DDX3Y mRNA expression was determined by a quantitative reverse transcriptase\u2010polymerase chain reaction. The interaction between miR\u2010497 and DDX3Y was verified by a luciferase reporter assay. Protein expression levels were tested by western blotting.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>CSE treatment decreased miR\u2010497 level in HBE cells. CSE exposure restrained cell proliferation, promoted cell apoptosis and enhanced the relative expression of TLR4 and p\u2010NF\u2010\u03baB p65. DDX3Y was predicted as a target of miR\u2010497. The mRNA and protein expression of DDX3Y was negatively modulated by miR\u2010497 in CSE\u2010injured HBE cells. Up\u2010regulation of miR\u2010497 by miR\u2010497 mimic increased cell proliferation and reduced cell apoptosis in CSE\u2010treated HBE cells, which were rescued by DDX3Y high expression in CSE\u2010treated HBE cells. Consistently, Bcl\u20102 protein level was heightened, whereas Bax and actived caspase\u20103\/9 protein levels were decreased by miR\u2010497 mimic in CSE\u2010stimulated HBE cells, which was reversed by DDX3Y over\u2010expression in CSE\u2010stimulated HBE cells. The relative expression of TLR4 and p\u2010NF\u2010\u03baB p65 was decreased by miR\u2010497 mimic, whereas they were rescued by DDX3Y over\u2010expression in CSE\u2010damaged HBE cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The results of the present study demonstrate that up\u2010regulation of miR\u2010497 exhibits a protective effect on CSE\u2010damaged HBE cells, which might be achieved by targeting DDX3Y and regulating the TLR4\/NF\u2010\u03baB pathway.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jgm.3137","type":"journal-article","created":{"date-parts":[[2019,11,7]],"date-time":"2019-11-07T10:58:06Z","timestamp":1573124286000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["MicroRNA\u2010497 functions as an inflammatory suppressor via targeting DDX3Y and modulating toll\u2010like receptor 4\/NF\u2010\u03baB in cigarette smoke extract\u2010stimulated human bronchial epithelial 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