101. microRNA-142-3p inhibits apoptosis and inflammation induced by bleomycin through down-regulation of Cox-2 in MLE-12 cells
- Author
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B. Yu, X.Y. Li, Q. Gao, D.J. Lin, S.C. Lin, F. Guo, and M.S. Zhao
- Subjects
0301 basic medicine ,Physiology ,Pro-inflammatory cytokines ,Immunology ,miR-142-3p ,Biophysics ,Down-Regulation ,Apoptosis ,Idiopathic pulmonary fibrosis ,Ocean Engineering ,Inflammation ,MLE-12 cells ,Transfection ,Bleomycin ,Biochemistry ,Cell Line ,Proinflammatory cytokine ,03 medical and health sciences ,chemistry.chemical_compound ,medicine ,Humans ,Viability assay ,General Pharmacology, Toxicology and Pharmaceutics ,Lung ,lcsh:QH301-705.5 ,Protein kinase B ,PI3K/AKT/mTOR pathway ,lcsh:R5-920 ,Chemistry ,General Neuroscience ,Biomedical Sciences ,Cell Biology ,General Medicine ,respiratory system ,Blot ,MicroRNAs ,030104 developmental biology ,lcsh:Biology (General) ,Cyclooxygenase 2 ,Cancer research ,medicine.symptom ,lcsh:Medicine (General) - Abstract
microRNA (miR)-142-3p is implicated in malignancy and has been identified as a biomarker for aggressive and recurrent lung adenocarcinomas. This study aimed to evaluate the inhibitory effect of miR-142-3p on apoptosis and inflammation induced by bleomycin in MLE-12 cells. MLE-12 cells were first transfected either with miR-142-3p mimic or miR-142-3p inhibitor and then the cells were exposed to 50 μg/mL of bleomycin. Thereafter, cell viability, apoptosis and the expression of pro-inflammatory cytokines were assessed using CCK-8, flow cytometry, RT-PCR and western blot analyses. Cox-2, PI3K, AKT and mTOR expressions were detected by western blotting after bleomycin was administered together with NS-398 (an inhibitor of Cox-2). As a result, cell viability was significantly decreased, as well as apoptosis and the expression of IL-1 and TNF-α were remarkably increased after 50 and 100 μg/mL of bleomycin administration. miR-142-3p overexpression alleviated bleomycin-induced apoptosis and overproduction of these two pro-inflammatory cytokines, while miR-142-3p suppression exhibited completely opposite results. Up-regulation of Cox-2 and inactivation of PI3K/AKT/mTOR were found in bleomycin-pretreated cells, while these abnormal regulations were partially abolished by miR-142-3p overexpression and NS-398. In conclusion, this study demonstrated that miR-142-3p overexpression protected bleomycin-induced injury in lung epithelial MLE-12 cells, possibly via regulating Cox-2 expression and PI3K/AKT/mTOR signaling pathway. These findings provide evidence that miR-142-3p may be a therapeutic strategy for idiopathic pulmonary fibrosis (IPF) treatment.
- Published
- 2017