title: [Interaction of protein kinase C-extracellular signal-regulated kinase 1/2 signal pathway in the process of plasminogen activator inhibitor-1 expression induced by nicotine in human umbilical vein endothelial cells].
abstract: OBJECTIVE
  To explore the role of protein kinase C (PKC)- extracellular signal-regulated kinase (ERK)1/2 signal pathway in the process of plasminogen activator inhibitor-1 (PAI-1) protein and mRNA expression in cultured human umbilical vein endothelial cells (HUVECs) induced by nicotine.
  
  
  METHODS
  HUVECs were cultured to examine the effect of nicotine on the expression of secreting PAI-1 in HUVECs on different experimental conditions. The expression of PAI-1 protein was measured by ELISA. PKC inhibitor staurosporine (STS) and ERK1/2 inhibitor PD98059 were used to detect PKC or ERK1/2 function on the expression of PAI-1 in HUVECs induced by nicotine. The PAI-1 mRNA expression was determined by RT-PCR.
  
  
  RESULTS
  The expression level of PAI-1 protein in 100 µmol/L nicotine treated group [(22.6 ± 1.1) µg/L] increased significantly compared to the control group [(14.2 ± 2.8) µg/L; q = 5.64, P < 0.05]. After stimulation with 100 µmol/L nicotine for 0, 4, 6, 8, 12 and 24 h, the levels of PAI-1 protein increased over time and reached the peak at 12 h (F = 32.063, P < 0.05). The PAI-1 mRNA and protein expression in nicotine treated group [(1.32 ± 0.20), (21.08 ± 0.83) µg/L] increased significantly compared to the control group [(0.73 ± 0.10), (13.39 ± 0.93) µg/L; q = 8.43, 11.97, all P < 0.05].Compared with nicotine treated group, the PAI-1 mRNA and protein expression in nicotine and STS treated group [(1.07 ± 0.10), (16.19 ± 2.15) µg/L] decreased significantly(q = 5.61, 7.61, all P < 0.05), but still higher than the control group (q = 7.84, 4.36, all P < 0.05). In nicotine and PD98059 treated group, the PAI-1 mRNA and protein expression [(1.12 ± 0.11), (17.52 ± 1.72) µg/L] decreased significantly compared to the nicotine treated group(q = 4.68, 5.54, all P < 0.05), still higher than the control group (q = 8.77, 6.43, all P < 0.05).
  
  
  CONCLUSIONS
  PKC-ERK1/2 signal pathway may play a partial role in the up-regulation of PAI-1 induced by nicotine in HUVECs.
authors.affiliation: Department of Respiratory Medicine, First Hospital, Shanxi Medical University, Taiyuan 030001, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: DU
authors.forename: Xiao-yun
authors.initials: XY
authors.lastname: Hu
authors.forename: Bao-fen
authors.initials: BF
authors.lastname: Han
authors.forename: Yong-cheng
authors.initials: YC
authors.lastname: DU
mesh_terms: D002478:Cells, Cultured; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects; D006801:Humans; D020935:MAP Kinase Signaling System; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D009538:Nicotine / Q000009:adverse effects*; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism*; D011493:Protein Kinase C / Q000378:metabolism*
chemical_list: D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D009538:Nicotine; D011493:Protein Kinase C; C535150:MAPK1 protein, human; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3