PMID- 16638301 OWN - NLM STAT- MEDLINE DCOM- 20100907 LR - 20121115 IS - 1001-0939 (Print) IS - 1001-0939 (Linking) VI - 29 IP - 1 DP - 2006 Jan TI - [Effects of sense vascular endothelial growth factor cDNA transfection on mononuclear chemotaxis protein-1 expression in rat pulmonary microvessel endothelial cells]. PG - 44-7 AB - 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). CONCLUSION: 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. FAU - Cui, Guang-bin AU - Cui GB AD - Department of Radiology, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China. FAU - Wei, Jing-guo AU - Wei JG FAU - Wang, Wei AU - Wang W FAU - Wei, Long-xiao AU - Wei LX FAU - Yin, Qian AU - Yin Q FAU - Yang, Hao AU - Yang H FAU - Huang, Xiao-feng AU - Huang XF LA - chi PT - English Abstract PT - Journal Article PL - China TA - Zhonghua Jie He He Hu Xi Za Zhi JT - Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases JID - 8712226 RN - 0 (Ccl2 protein, rat) RN - 0 (Chemokine CCL2) RN - 0 (DNA, Complementary) RN - 0 (RNA, Messenger) RN - 0 (Vascular Endothelial Growth Factor A) RN - 0 (vascular endothelial growth factor A, rat) SB - IM MH - Animals MH - Chemokine CCL2/genetics/*metabolism MH - DNA, Complementary/genetics MH - Endothelial Cells/*metabolism MH - Genetic Therapy MH - Pulmonary Fibrosis/*metabolism MH - RNA, Messenger/genetics MH - Rats MH - Rats, Sprague-Dawley MH - Tight Junctions/metabolism MH - *Transfection MH - Vascular Endothelial Growth Factor A/*genetics EDAT- 2006/04/28 09:00 MHDA- 2010/09/08 06:00 CRDT- 2006/04/28 09:00 PHST- 2006/04/28 09:00 [pubmed] PHST- 2010/09/08 06:00 [medline] PHST- 2006/04/28 09:00 [entrez] PST - ppublish SO - Zhonghua Jie He He Hu Xi Za Zhi. 2006 Jan;29(1):44-7.