Peilin Cui , Bing Chen, Minghua Yu, Zhaohua Luo , Yan Su and Ruijuan Xiu
Connective tissue growth factor (CTGF), a member of the CCN (Cyr61, Ctgf, Nov) family, is involved in many biological processes such as angiogenesis. In this study we analyzed the action of CTGF in transfected human umbilical vein endothelial cells (HUVECs) and explored the possible mechanism. The eukaryotic expression vector of CTGF gene was constructed in this study, and cDNA was amplified from HUVECs. The expression vector (pcDNA3.1 (-)/CTGF) which contains the entire coding region was verified by DNA sequence analysis and transferred successfully into HUVECs. Western blot analysis demonstrated that CTGF protein in HUVECs was over-expressed at 48h after transfection. To elucidate the putative mechanism of CTGF�?¢�?�?��?�?�s transfection on HUVEC proliferation, the intracellular signaling pathways included mitogen-activated protein kinases (MAPK) and phosphoinositol 3-kinase (PI3K)/Akt were detected. The results demonstrated CTGF transfection promoted the proliferation of HUVECs; ERK1/2 and PI3K/Akt activities were increased when HUVECs transfected with CTGF; Special inhibitors (LY294002 and U0126) could partially prevent the pro-proliferative action of CTGF transfection. In conclusion, our data showed that CTGF transfection promoted the proliferation of HUVECs, and the ERK1/2 and Akt signal pathways involved in.
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