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Des-γ-carboxy prothrombin increase the proliferation and migration of human vascular endothelial cells
Li Yuanyuan 1,Yuan Yi 2,Qu Xianjun 2 *
1.Department of Pharmacology, School of Pharmaceutical Science, JiNan 250012
2.Department of Pharmacology, School of Pharmaceutical Science
*Correspondence author
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Funding: none
Opened online:14 January 2013
Accepted by: none
Citation: Li Yuanyuan,Yuan Yi,Qu Xianjun.Des-γ-carboxy prothrombin increase the proliferation and migration of human vascular endothelial cells[OL]. [14 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4511380
 
 
Des-γ-carboxy prothrombin (DCP) is an aberrant prothrombin produced by hepatocellular carcinoma (HCC) cells. High level of DCP in serum and tissue is considered to show the malignant potential of HCC. In this paper, we described the proliferation and migration of human vascular endothelial cells by DCP. MTT assay showed that DCP could significantly stimulate HUVEC ECV304 cell proliferation with dose and time dependent manner. A continuous rapid migration of ECV304 cells was seen after treatment with DCP as measured by the scratch wound assay. A continuous rapid invasive activity as evaluated by transwell chamber assay also showed that DCP increased endothelial cells migration through the reconstituted extracellular matrix. The tube formation of vascular endothelial cells on 3-D Matrigel showed an increase of branch points of ECV304 cells exposed to DCP. The expressions of vascular endothelial cell growth-related angiogenic factors and matrix metalloproteinase were examined by Western blotting assay. DCP significantly stimulated the expression levels of epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and matrix metalloproteinase (MMP)-2 (latent and active). Together, these results suggest that DCP is a vascular endothelial growth factor. DCP may play a crucial role of mitogenic and migrative activities in angiogenesis in the development of HCC.
Keywords:HCC; DCP; human vascular endothelial cell; angiogenesis; EGFR; VEGF; MMPs
 
 
 

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