title: [Effects of sense vascular endothelial growth factor cDNA transfection on mononuclear chemotaxis protein-1 expression in rat pulmonary microvessel endothelial cells].
abstract: OBJECTIVE
  To study the transformation characteristics of tight junction of microvessel endothelial cells in bleomycin (BLM) induced pulmonary fibrosis (PF), and the effects of vascular endothelial growth factor (VEGF) on mononuclear chemotaxis protein-1 (MCP-1) mRNA expression in pulmonary microvessel endothelial cells (EC).
  
  
  METHODS
  Forty healthy rats were equally divided into a control and an experimental group in random. In the experimental group, PF were induced by BLM application. In each group, 10 rats were instilled by lanthanum sal at 3, 7, 14 and 28 d after BLM application, and lung samples were made and observed by transmission electron microscopy. The pulmonary microvessel EC of the other 10 rats in each group were preserved by tissue culture methods at the same time, and the cells were transfected with sense VEGF cDNA, and then MCP-1 mRNA expression was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) technique.
  
  
  RESULTS
  Blood vessel endothelial cells of the control group were intact. The basement membrane was shown as a continuous line. Granules of lanthanum sal did not cross the tight junction of endothelial cells. The width of the junction gap in rats of the experimental group treated at different times was increased and lanthanum particles of high density were seen in the gap junction, particularly on day 3, and were distributed in the area of subendothelium. The MCP-1 mRNA expression in VEGF transfected microvessel EC was significantly higher than that of the control group (1.21 +/- 0.22 vs 0.36 +/- 0.06, P < 0.05).
  
  
  CONCLUSIONS
  In BLM induced PF, the opening of the tight junction of EC, and the high expression of MCP-1 induce inflammatory cell infiltration and cytokine over-secretion, which in turn enhances proliferation of fibroblasts, one of the important factors underlying lung fibrosis.
authors.affiliation: Department of Radiology, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
authors.forename: Guang-bin
authors.initials: GB
authors.lastname: Cui
authors.forename: Jing-guo
authors.initials: JG
authors.lastname: Wei
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Long-xiao
authors.initials: LX
authors.lastname: Wei
authors.forename: Qian
authors.initials: Q
authors.lastname: Yin
authors.forename: Hao
authors.initials: H
authors.lastname: Yang
authors.forename: Xiao-feng
authors.initials: XF
authors.lastname: Huang
mesh_terms: D000818:Animals; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism*; D018076:DNA, Complementary / Q000235:genetics; D042783:Endothelial Cells / Q000378:metabolism*; D015316:Genetic Therapy; D011658:Pulmonary Fibrosis / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D019108:Tight Junctions / Q000378:metabolism; D014162:Transfection; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics*
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D018076:DNA, Complementary; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat