title: [Detection of the mRNA level of the subunits of amiloride-sensitive Na+ channel in human bronchial epithelium cells from patients with chronic obstructive pulmonary disease].
abstract: OBJECTIVE
  To investigate the role of epithelial amiloride-sensitive Na(+) channel (ENaC) in the pathogenesis of chronic obstructive pulmonary disease (COPD) and the effect of interleukin-4 (IL-4) and IL-6.
  
  
  METHODS
  Human bronchial epithelial cells were isolated and cultured from 18 patients who undergone pneumonectomy in Tongji hospital. The patients were allocated into COPD group, smoking group and control group based on their lung functions and smoking history, with 6 patients in each group. IL-4 and IL-6 were added to the primary cultured human bronchial epithelial cells, and reverse transcriptase-polymerase chain reaction (RT-PCR) was preformed to detect mRNA of ENaC subunits alpha, beta and gamma.
  
  
  RESULTS
  ENaC alpha subunit mRNA was found increased in the smoking group (0.322 +/- 0.041) and the COPD group (0.314 +/- 0.042), and gamma ENaC subunits were found up-regulated in the COPD group (0.585 +/- 0.045, P < 0.05); IL-4 could up-regulate ENaC alpha subunit mRNA (0.382 +/- 0.025, 0.385 +/- 0.047, 0.412 +/- 0.067, respectively) and decrease beta subunit (0.319 +/- 0.030, 0.307 +/- 0.207, 0.281 +/- 0.029, respectively), gamma subunit (0.396 +/- 0.063, 0.359 +/- 0.038, 0.481 +/- 0.049, respectively) mRNA in all groups (P < 0.05), while IL-6 only increased ENaC alpha subunit mRNA in the smoking group (0.125 +/- 0.040) and decreased beta, gamma subunit mRNA in the COPD group (0.346 +/- 0.041, 0.442 +/- 0.047, respectively; P < 0.05).
  
  
  CONCLUSIONS
  The increased ENaC alpha and gamma subunits in COPD group suggest that they may play a key role in the pathogenesis of COPD. Similarly, the increased ENaC alpha subunit mRNA in the smoking group indicates that smoking contributes to COPD development. IL-4 and IL-6 can influence the re-absorption of Na(+) in bronchial epithelial cells, which may be involved in the hypersecretion of COPD.
authors.affiliation: Department of Respiratory Medicine, Tongji Hospital of Tongji Medical College, Huazhong Science and Technology University, Wuhan 430030, China.
authors.forename: Wen
authors.initials: W
authors.lastname: Li
authors.forename: Yong-jian
authors.initials: YJ
authors.lastname: Xu
authors.forename: Zhen-xiang
authors.initials: ZX
authors.lastname: Zhang
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D001980:Bronchi / Q000166:cytology / Q000378:metabolism*; D002478:Cells, Cultured; D004847:Epithelial Cells / Q000378:metabolism; D053503:Epithelial Sodium Channels; D005260:Female; D006801:Humans; D015847:Interleukin-4 / Q000494:pharmacology*; D015850:Interleukin-6 / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis; D015222:Sodium Channels / Q000096:biosynthesis* / Q000235:genetics; D015854:Up-Regulation
chemical_list: D053503:Epithelial Sodium Channels; D015850:Interleukin-6; D012333:RNA, Messenger; D015222:Sodium Channels; D015847:Interleukin-4; D000584:Amiloride