利用微泡超声破坏技术将VEGF介导的血管生成靶向作用于大鼠心肌。
Targeting of VEGF-mediated angiogenesis to rat myocardium using ultrasonic destruction of microbubbles.
作者信息
Korpanty G, Chen S, Shohet R V, Ding J, Yang B, Frenkel P A, Grayburn P A
机构信息
Division of Cardiology, University of Texas Southwestern Medical School, Dallas, TX 75226, USA.
出版信息
Gene Ther. 2005 Sep;12(17):1305-12. doi: 10.1038/sj.gt.3302532.
Myocardial angiogenesis mediated by human vascular endothelial growth factor 165 (hVEGF165) cDNA was promoted in rat myocardium using an in vivo-targeted gene delivery system known as ultrasound-targeted microbubble destruction (UTMD). Microbubbles carrying plasmids encoding hVEGF165, or control solutions were infused intravenously during ultrasonic destruction of the microbubbles within the myocardium. Biochemical and histological assessment of gene expression and angiogenesis were performed 5, 10, and 30 days after UTMD. UTMD-treated myocardium contained hVEGF165 protein and mRNA. The myocardium of UTMD-treated animals showed hypercellular foci associated with hVEGF165 expression and endothelial cell markers. Capillary density in UTMD-treated rats increased 18% at 5 days and 33% at 10 days, returning to control levels at 30 days (P<0.0001). Similarly, arteriolar density increased 22% at 5 days, 86% at 10 days, and 31% at 30 days (P<0.0001). Thus, noninvasive delivery of hVEGF165 to rat myocardium by UTMD resulted in significant increases in myocardial capillary and arteriolar density.
利用一种名为超声靶向微泡破坏（UTMD）的体内靶向基因递送系统，在大鼠心肌中促进了由人血管内皮生长因子165（hVEGF165）cDNA介导的心肌血管生成。在超声破坏心肌内的微泡过程中，静脉注射携带编码hVEGF165的质粒的微泡或对照溶液。在UTMD后5天、10天和30天对基因表达和血管生成进行生化和组织学评估。UTMD处理的心肌含有hVEGF165蛋白和mRNA。UTMD处理动物的心肌显示出与hVEGF165表达和内皮细胞标志物相关的细胞增多灶。UTMD处理的大鼠的毛细血管密度在5天时增加18%，在10天时增加33%，在30天时恢复到对照水平（P<0.0001）。同样，小动脉密度在5天时增加22%，在10天时增加86%，在30天时增加31%（P<0.0001）。因此，通过UTMD将hVEGF165无创递送至大鼠心肌导致心肌毛细血管和小动脉密度显著增加。
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