title: [Apoptosis versus proliferation activities and relative mechanism in chronic obstructive pulmonary disease].
abstract: OBJECTIVE
  To study the roles of apoptosis and proliferation and relative genes expression in chronic obstructive pulmonary disease (COPD) and pulmonary hypertension.
  
  
  METHODS
  Immunohistochemical technique was used for the detection of cell proliferation and expression of relative genes. In situ end labeling technique was used for the detection of nucleosomal DNA fragmentation of apoptotic cells, and Northern blot for the detection of expression of c-myc, bcl-2 and p53 genes in the lungs with COPD.
  
  
  RESULTS
  Both proliferative cells and apoptotic cells were found in the lungs with COPD or without COPD. In lung tissue with COPD. The proliferation index was increased significantly, whereas the apoptosis index was decreased significantly. Compared with controls, the ratio of proliferation to apoptosis in lungs with COPD was increased by 4 folds, and the expression of c-myc or bcl-2 mRNA was significantly increased by 2.5-3 folds in lungs tissue with COPD. The expression of c-myc and bcl-2 protein was also increased significantly in lungs with COPD, the two antigen were predominantly localized in small pulmonary vessels. The expression of p53 mRNA was significantly decreased by 3 folds in lung tissue with COPD.
  
  
  CONCLUSIONS
  The abnormality of apoptosis versus proliferation activities induced by c-myc, bcl-2 and p53 genes may contribute to pulmonary vascular structural remodeling in COPD.
authors.affiliation: Respiratory Disease Research Laboratory, Tongji Hospital, Tongji Medical University, Wuhan.
authors.forename: Q
authors.initials: Q
authors.lastname: Tao
authors.forename: Z
authors.initials: Z
authors.lastname: Zhang
authors.forename: Y
authors.initials: Y
authors.lastname: Xu
mesh_terms: D017209:Apoptosis; D001158:Arteries / Q000473:pathology; D002455:Cell Division; D005260:Female; D019254:Genes, bcl-2; D016259:Genes, myc; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000235:genetics; D008168:Lung / Q000098:blood supply / Q000473:pathology*; D008173:Lung Diseases, Obstructive / Q000235:genetics / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*
chemical_list: D016159:Tumor Suppressor Protein p53