论文部分内容阅读
目的研究缺血肌肉转染腺病毒(Ad)携带人血管内皮细胞生长因子165(VEGF-165)和人血管形成素-1(Ang-1)基因后引起的细胞动员效应。方法制作大鼠下肢血管闭塞模型,肌肉内注射Ad5VEGF-165和/或Ad5Ang-1,以Western法检测生长因子蛋白表达、免疫组化检测基因导入后在缺血肌肉引起的效应。结果(1)局部转基因肌肉组织高表达人VEGF-165蛋白和人Ang1蛋白;(2)与对照组相比,接收两因子转染后的骨骼肌纤维间溴化脱氧尿嘧啶(BrdU)阳性的浸润细胞显著增多,呈协同效应。有细胞同时表达内皮细胞、骨骼肌细胞、平滑肌细胞标志性抗原。部分细胞表达CD117+并分化为新生微血管的内皮细胞。结论(1)两因子能促进CD117+骨髓干细胞动员到缺血组织部位并分化为内皮细胞参与血管新生;(2)两因子可能协同动员召集能在缺血部位聚集并分化为其它类型细胞的干/祖细胞;(3)两因子可能同时作为血管生成因子和细胞动员剂用于缺血性疾病的干细胞移植治疗中,以增强缺血损伤修复效果和节省干细胞用量。
Objective To investigate the cell mobilization induced by recombinant adenovirus carrying human vascular endothelial growth factor 165 (VEGF-165) and human angiopoietin-1 (Ang-1) gene. Methods The rat model of lower extremity vascular occlusion was established. Ad5 VEGF-165 and / or Ad5Ang-1 were injected intramuscularly. The expression of growth factor protein was detected by Western blot. The effect induced by ischemic muscle was detected by immunohistochemistry. Results (1) Local genetically modified muscle tissue highly expressed human VEGF-165 protein and human Ang1 protein. (2) BrdU-positive infiltration of skeletal muscle fibers Cells significantly increased, showing a synergistic effect. Some cells also express endothelial cells, skeletal muscle cells, smooth muscle cell marker antigen. Some cells express CD117 + and differentiate into endothelial cells of the neovascular microvasculature. Conclusions (1) The two factors can promote the mobilization of CD117 + bone marrow stem cells to ischemic tissue and differentiation into endothelial cells involved in angiogenesis; (2) two factors may be coordinated mobilization called in the ischemic area and differentiation into other types of cells dry / Progenitor cells; (3) two factors may serve as angiogenesis factors and cell mobilization agent for the treatment of ischemic diseases in stem cell transplantation to enhance the repair effect of ischemic injury and save the amount of stem cells.