title: [Induction effect of platelet-activating factor on Src-suppressed C kinase substrate gene expression in rat pulmonary microvascular endothelial cells].
abstract: OBJECTIVE
  To investigate the effect of platelet-activating factor (PAF) on the production of Src-suppressed C kinase substrate (SSeCKS) mRNA in rat pulmonary microvascular endothelial cell (RPMVEC) and its signal transduction pathways.
  
  
  METHODS
  Cellular in situ hybridization was performed to reveal changes in SSeCKS mRNA expression in the cultured RPMVECs after giving PAF stimulation.
  
  
  RESULTS
  Normal RPMVECs expressed SSeCKS mRNA at a low level, which appeared throughout the cytoplasm with specific hybridization signals. 1.5 hours of 10(-10), 10(-9), 10(-8), 10(-7) mol/L PAF incubation induced a progressive increase in SSeCKS mRNA expression. When compared to the normal control group each difference had statistical significance (0.054 9 + or - 0.000 7, 0.059 9 + or - 0.001 8, 0.069 0 + or - 0.001 8, 0.075 4 + or - 0.001 9 vs. 0.036 8 + or - 0.003 7, respectively, all P<0.05). Within 0.5, 1.5, 3, 6, 12, 24 hours of 10(-7) mol/L PAF challenge, the level of SSeCKS mRNA expression raised at 0.5 hour markedly (0.071 0 + or - 0.001 5), peaked at 1.5 hours (0.075 6 + or - 0.001 7), then began to decline gradually, and still persisted at a higher level than the normal control group until 24 hours (0.043 9 + or - 0.001 0 vs. 0.038 2 + or - 0.004 1, all P<0.05). Pre-incubation of 10 micromol/L pyrrolidine dithiocarbamate (PDTC) that inhibits activity of nuclear factor-KappaB (NF-KappaB) in RPMVECs caused a conspicuous attenuation of PAF-induced SSeCKS mRNA expression (0.049 7 + or - 0.003 2 vs. 0.071 9 + or - 0.001 9, P<0.05), whereas no change of PAF-induced effect was found by pretreatment of protein kinase C (PKC) inhibitor bis-indolylmaleimide (BIM, 0.069 7 + or - 0.002 1 vs. 0.071 9 + or - 0.001 9, P>0.05).
  
  
  CONCLUSIONS
  PAF can up regulate the expression of SSeCKS mRNA in a dose- and time-dependent manner in RPMVECs. It is NF-KappaB rather than PKC signal pathway that is involved in modulation of the intracellular signaling process.
authors.affiliation: Department of Respiratory Medicine, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui, China.
authors.forename: Shan
authors.initials: S
authors.lastname: Chen
authors.forename: Geng-yun
authors.initials: GY
authors.lastname: Sun
authors.forename: Qing-hai
authors.initials: QH
authors.lastname: You
authors.forename: Nan
authors.initials: N
authors.lastname: Wang
mesh_terms: D054758:A Kinase Anchor Proteins / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D002196:Capillaries / Q000166:cytology; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism*; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000166:cytology; D015870:Gene Expression / Q000187:drug effects; D008168:Lung / Q000098:blood supply; D010972:Platelet Activating Factor / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D054758:A Kinase Anchor Proteins; C102361:Akap12 protein, rat; D018797:Cell Cycle Proteins; D010972:Platelet Activating Factor; D012333:RNA, Messenger