title: [A study of the effect of protein kinase C on the expression of nitric oxide synthase mRNA in pulmonary artery smooth muscle in hypoxia].
abstract: OBJECTIVE
  To investigate the effect of PKC on the expression of NOS mRNA in pulmonary artery smooth muscle cell(PASMC) in hypoxia.
  
  
  METHODS
  RT-PCR was used to detect the expression of PKC alpha mRNA in PASMC of procine, and the effect of activator and inhibitor of PKC on the expression of cNOS mRNA in PASMC.
  
  
  RESULTS
  The expression of PKC-alpha mRNA was higher in the PASMC in 48 and 72 h of hypoxia(P < 0.01), and the expression of cNOS mRNA was lower(P < 0.01). The expression of cNOS mRNA was significantly negatively correlated with the expression of PKC-alpha mRNA(P < 0.001). PMA, an agonist of PKC could reduce the expression of cNOS mNRA in hypoxia, while RO 31-8220, an inhibitor of PKC could inhibit it and enhance the expression of NOS mRNA(P < 0.01). The activator of NO, L-Arg and inhibitor, L-NAME had no effect on expression of PKC-alpha mRNA.
  
  
  CONCLUSIONS
  The PKC can inhibit the expression of cNOS mRNA in PASMC in hypoxia. The effect of PKC in hypoxic pulmonary hypertension may be made by inhibiting the expression of cNOS mRNA and modulating NO. The site of the effect of PKC may be in upstream of NO. The mechanism of it needs to be studied further.
authors.affiliation: Department of Respiratory Disease, Tongji Hospital, Tongji Medical College, Huazhong Science and Technology University, Wuhan 430030, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Ding
authors.forename: Y
authors.initials: Y
authors.lastname: Xu
authors.forename: Z
authors.initials: Z
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001120:Arginine / Q000494:pharmacology; D015687:Cell Hypoxia; D002478:Cells, Cultured; D004791:Enzyme Inhibitors / Q000494:pharmacology; D015870:Gene Expression; D007211:Indoles / Q000494:pharmacology; D007527:Isoenzymes / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000201:enzymology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000235:genetics*; D052250:Nitric Oxide Synthase Type III; D010100:Oxygen / Q000378:metabolism; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051571:Protein Kinase C-alpha; D011651:Pulmonary Artery / Q000166:cytology / Q000201:enzymology*; D012333:RNA, Messenger; D013552:Swine; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013997:Time Factors
chemical_list: D004791:Enzyme Inhibitors; D007211:Indoles; D007527:Isoenzymes; D012333:RNA, Messenger; D001120:Arginine; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D011493:Protein Kinase C; D051571:Protein Kinase C-alpha; D013755:Tetradecanoylphorbol Acetate; D010100:Oxygen; D019331:NG-Nitroarginine Methyl Ester; C064758:Ro 31-8220