title: [Regulatory effect of miR-149 on interleukin-6 expression in silica-induced pulmonary fibrosis].
abstract: OBJECTIVE
  To investigate the regulatory effect of miR-149 on interleukin-6 (IL-6) expression in silica-induced pulmonary fibrosis.
  
  
  METHODS
  A mouse model of pulmonary fibrosis was established using silica dust; the level of miR-149 in the lung tissues of mice with silica-induced pulmonary fibrosis was measured by quantitative real-time polymerase chain reaction (qRT-PCR), while the protein expression of IL-6 was measured by immunohistochemistry and Western blot. Type II alveolar epithelial cells (A549) and bronchial epithelial cells (HBE) were exposed to silica dust to establish a model; the level of miR-149 was measured by qRT-PCR, while the protein expression of IL-6 was measured by Western blot. A549 cells were transfected with miR-149 mimics and inhibitor in vitro, and the cellular expression of IL-6 was measured by Western blot. Serum samples from patients with coal workers' pneumoconiosis were examined by double-antibody sandwich ELISA to measure the protein expression of IL-6.
  
  
  RESULTS
  At three time points after silica treatment, the miR-149 expression in lung tissues was significantly down-regulated while an evident increase in IL-6 expression was observed in lung tissues (P < 0.01). Silica-stimulated epithelial cell (A549 and HBE) had up-regulated IL-6 expression and down-regulated miR-149 expression (P < 0.01). Increased levels of miR-149 attenuated IL-6 expression, whereas adverse results were found when miR-149 was inhibited. Compared with that in control group, serum level of IL-6 was significantly increased in patients with stage II and III coal workers' pneumoconiosis (P < 0.01).
  
  
  CONCLUSIONS
  Down-regulation of miR-149 and up-regulation of IL-6 might be involved in the progression of silica-induced pulmonary fibrosis; miR-149 could negatively regulate IL-6 expression.
authors.affiliation: Department of Occupational Medicine and Environmental Health, School of Public Health, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Jingjing
authors.initials: J
authors.lastname: Fan
authors.affiliation: Department of Occupational Medicine and Environmental Health, School of Public Health, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Xiaoming
authors.initials: X
authors.lastname: Ji
authors.affiliation: Department of Occupational Medicine and Environmental Health, School of Public Health, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Shasha
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Occupational Medicine and Environmental Health, School of Public Health, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Chen
authors.initials: C
authors.lastname: Luo
authors.affiliation: Department of Occupational Medicine and Environmental Health, School of Public Health, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Baiqun
authors.initials: B
authors.lastname: Wu
authors.affiliation: Department of Occupational Medicine and Environmental Health, School of Public Health, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Ting
authors.initials: T
authors.lastname: Wang
authors.affiliation: Department of Occupational Medicine and Environmental Health, School of Public Health, Nanjing Medical University, Nanjing 210029, China. E-mail: chni@njmu.edu.cn.
authors.forename: Chunhui
authors.initials: C
authors.lastname: Ni
mesh_terms: D000818:Animals; D055008:Anthracosis / Q000097:blood*; D002478:Cells, Cultured; D004195:Disease Models, Animal; D006801:Humans; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000378:metabolism*; D011658:Pulmonary Fibrosis / Q000139:chemically induced*; D012822:Silicon Dioxide / Q000633:toxicity*
chemical_list: D015850:Interleukin-6; D035683:MicroRNAs; C570833:Mirn15 microRNA, mouse; D012822:Silicon Dioxide