%0 Journal Article %1 Dong.2009 %A Dong, H. %A Wang, Q. %A Zhang, Y. %A Jiang, B. %A Xu, X. %A Zhang, Z. %D 2009 %J Exp.Biol.Med.(Maywood.) %K 1 A Actins Animals Antigens Blood CD31 Dependovirus Elements Endothelial Expression Factor Gene Genetic Growth Heart Human Humans Hypoxia-Inducible Immunohistochemistry Ischemia Myocardial Myocardium Neovascularization Physiologic Rabbits Regulation Research Response Subunit Therapy Transduction Vascular Vessels alpha biosynthesis blood genetics pathology protein response therapy %N 12 %P 1417-1424 %T Angiogenesis induced by hVEGF165 gene controlled by hypoxic response elements in rabbit ischemia myocardium %U PM:19934363 %V 234 %X Hypoxic response element (HRE) offers satisfactory control over expression of hVEGF(165) in cell levels. However, the characteristics of regenerated blood vessels induced by long-term expression of transferred hVEGF(165) under control of HRE in vivo remain unknown. This study aims to investigate the effect of HRE on control of long-term expression of rAAV-delivered hVEGF(165) gene to ischemic myocardium and evaluate characteristics of angiogenesis induced by hVEGF(165) in vivo. Rabbit ischemic heart models were established surgically, rAAV-9HRE-hVEGF(165) was transfected to ischemia hearts subjected to 12 week ischemia. Molecular biological and immunohistochemistry were employed to determine expressions of HIF-1alpha and hVEGF(165). Microvessel densities of CD31(+) and alpha-SMA(+) regenerated vessels were also evaluated. Expressions of both hVEGF(165) mRNA and protein were upregulated following over-expression of endogenous HIF-1alpha early after ischemia, peaked at 4-6 weeks post-MI,

@article{Dong.2009, abstract = {Hypoxic response element (HRE) offers satisfactory control over expression of hVEGF(165) in cell levels. However, the characteristics of regenerated blood vessels induced by long-term expression of transferred hVEGF(165) under control of HRE in vivo remain unknown. This study aims to investigate the effect of HRE on control of long-term expression of rAAV-delivered hVEGF(165) gene to ischemic myocardium and evaluate characteristics of angiogenesis induced by hVEGF(165) in vivo. Rabbit ischemic heart models were established surgically, rAAV-9HRE-hVEGF(165) was transfected to ischemia hearts subjected to 12 week ischemia. Molecular biological and immunohistochemistry were employed to determine expressions of HIF-1alpha and hVEGF(165). Microvessel densities of CD31(+) and alpha-SMA(+) regenerated vessels were also evaluated. Expressions of both hVEGF(165) mRNA and protein were upregulated following over-expression of endogenous HIF-1alpha early after ischemia, peaked at 4-6 weeks post-MI,}, added-at = {2010-02-05T11:28:39.000+0100}, author = {Dong, H. and Wang, Q. and Zhang, Y. and Jiang, B. and Xu, X. and Zhang, Z.}, biburl = {https://www.bibsonomy.org/bibtex/2ae12b8b83cbe6601583e2988c0987828/kanefendt}, interhash = {a213ce39ffcd119483ea58da2ac44929}, intrahash = {ae12b8b83cbe6601583e2988c0987828}, journal = {Exp.Biol.Med.(Maywood.)}, keywords = {1 A Actins Animals Antigens Blood CD31 Dependovirus Elements Endothelial Expression Factor Gene Genetic Growth Heart Human Humans Hypoxia-Inducible Immunohistochemistry Ischemia Myocardial Myocardium Neovascularization Physiologic Rabbits Regulation Research Response Subunit Therapy Transduction Vascular Vessels alpha biosynthesis blood genetics pathology protein response therapy}, number = 12, pages = {1417-1424}, timestamp = {2010-02-05T11:28:52.000+0100}, title = {Angiogenesis induced by hVEGF165 gene controlled by hypoxic response elements in rabbit ischemia myocardium}, url = {PM:19934363}, volume = 234, year = 2009 }