title: [The effect of hypoxia on pulmonary artery smooth muscle cells two pore domain potassium channels TASK-1 and the regulation of non-receptor tyrosine kinases].
abstract: OBJECTIVE
  To investigate the effect of hypoxia on the human pulmonary artery smooth muscle cells two pore domain potassium channels TASK-1 and the regulation of non-receptor tyrosine kinase c-Src in this process.
  
  
  METHODS
  The cultured human pulmonary artery smooth muscle cells (hPASMCs) were divided into: normal group, hypoxia 30 minute group, hypoxia 6 hours group and hypoxia 48 hour group, and hypoxia 48 hour + PP2 group, hypoxia 48 hour + PP3 group, hypoxia 48 hour + bpV group. Flow cytometry was used to analyze the cell cycle, RT-PCR and Western blot technique were carried out to detect the expression changes of TASK-1 mRNA and protein in different groups.
  
  
  RESULTS
  (1) Cell Cycle Show: Compared with normal control group, with prolonged hypoxia, the percentages of hPASMCs in S phases of cell cycle were increased. While compared with hypoxia 48 hour group, the percentages of hypoxia 48 hour + PP2 group hPASMCs in S phases of cell cycle were decreased. The expression of TASK-1 mRNA on hPASMCs in acute hypoxia 6 hour group was increased, while the expression of TASK-1 protein on hPASMCs in the acute and chronic hypoxia group was decreased, and the expression of TASK-1 mRNA on hPASMCs in the chronic hypoxia group was decreased; After pre-incubation of a potent and selective inhibitor of the Src family of protein tyrosine kinases PP2, the expression of TASK-1 mRNA and protein in hypoxia 48 hour group was increased, however after pre-incubation of the inhibitor of the Src family of protein tyrosine phosphatase bpV, the expression of TASK-1 protein in hypoxia 48 hour group was decreased.
  
  
  CONCLUSIONS
  Hypoxia promotes human pulmonary artery smooth muscle cell proliferation, and non-receptor tyrosine kinase c-Src may participate in the expression of two pore domain potassium channels TASK-1 regulated by hypoxia. Therefore, we hypothesized that TASK-1 channels and c-Src participatein the acute and chronic hypoxic human pulmonary vasoconstriction.
authors.forename: Zhen
authors.initials: Z
authors.lastname: Tian
authors.forename: Bi
authors.initials: B
authors.lastname: Tang
authors.forename: Xin
authors.initials: X
authors.lastname: Cai
authors.forename: Chao
authors.initials: C
authors.lastname: Shi
authors.forename: Hong-ju
authors.initials: HJ
authors.lastname: Wang
authors.forename: Xiu-jie
authors.initials: XJ
authors.lastname: Hou
mesh_terms: D000081247:CSK Tyrosine-Protein Kinase; D015687:Cell Hypoxia; D049109:Cell Proliferation; D002478:Cells, Cultured; D006801:Humans; D032389:Myocytes, Smooth Muscle / Q000166:cytology*; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D024683:Potassium Channels, Tandem Pore Domain / Q000378:metabolism*; D011651:Pulmonary Artery / Q000166:cytology; D012333:RNA, Messenger; D014661:Vasoconstriction; D019061:src-Family Kinases / Q000378:metabolism*
chemical_list: D009419:Nerve Tissue Proteins; D024683:Potassium Channels, Tandem Pore Domain; D012333:RNA, Messenger; C420132:potassium channel subfamily K member 3; D000081247:CSK Tyrosine-Protein Kinase; D019061:src-Family Kinases; C000631346:CSK protein, human