Expression of Soluble Vascular Endothelial Growth Factor Receptor-2 and Its Effect on Proliferation of Vascular Endothelial Cells
Expression of Soluble Vascular Endothelial Growth Factor Receptor-2 and Its Effect on Proliferation of Vascular Endothelial Cells作者机构:The Seconal Hospital of Jilin UniversityChangchun 130041P.R.China China-Japan Union Hospital of Jilin UniversityChangchun 130033P.R.China The First Hospital of Jilin UniversityChangchun 130021P.R.China
出 版 物:《Chemical Research in Chinese Universities》 (高等学校化学研究(英文版))
年 卷 期:2012年第28卷第2期
页 面:245-248页
核心收录:
学科分类:0710[理学-生物学] 07[理学] 0905[农学-畜牧学] 09[农学] 071007[理学-遗传学] 090501[农学-动物遗传育种与繁殖]
基 金:国家自然科学基金
主 题:Kinase insert domain-containing receptor(KDR) Angiogenesis Human umbilical vein endothelial cell(HUVEC) Chick chorioallantoic membrane(CAM)
摘 要:Vascular endothelial growth factors(VEGFs) respectively bind to each of three receptor tyrosine kinases(RTKs),known as Flt-1,KDR and *** VEGFs and their respective families of receptor tyrosine kinases(VEGFRs) are critical proteins which can regulate vascular development during angiogenesis,we decided to explore the inhibitory effects of soluble kinase insert domain-containing receptor(sKDR) on endothelial cells and *** RNA was extracted from human umbilical vein endothelial cells(HUVEC),and cDNA of extracellular domains 1―4 was amplified and recombined with pQE40 *** being expressed,affinity purified,renatured and analyzed by Western blot,the sKDR was assayed for its effects on endothelial cells by [3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide](MTT),and on angiogenesis by chick chorioallantoic membrane(CAM) *** cDNA of 1150 bp was obtained via real-time polymerase chain reaction(RT-PCR),and sKDR was expressed by pQE40 procaryotic expression system,purified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis(SDS-PAGE) analysis with only one band and proved by Western *** assay demonstrateds that sKDR could inhibit the VEGF-stimulated HUVEC from proliferation,and CAM experiment showed sKDR could block the VEGF-induced *** has the biological activity to bind with VEGF ligands and is a potential target for tumor anti-angiogenesis therapy.