Objective： To investigate the effects of basic transcriptional element binding protein-2 （BTEB2） antisense RNA on vascular smooth muscle cells （VSMCs） proliferation and the neointimal formation after carotid ball...Objective： To investigate the effects of basic transcriptional element binding protein-2 （BTEB2） antisense RNA on vascular smooth muscle cells （VSMCs） proliferation and the neointimal formation after carotid balloon injury in rats. Methods： The cultured VSMCs were transfected with an adenoviral vector containing BTEB2 antisense gene, Ad ASBTEB2. Effects of BTEB2 antisense RNA on the expression of BTEB2 were investigated by Western blot analysis. The cell cycle was analyzed using flow cytometry. Ad ASBTEB2, control adenoviral vector Ad. LacZ or PBS was transduced into the rat carotid artery after balloon injury. The expression of BTEB2 at 7, 14, and 21 d after gene transfer was detected by immunohistochemistry and neointima-to-media （I/M） area ratio at these time points was calculated. Resuits： The cell cycle was arrested in G0/G1 phase and the expression of BETB2 was downregulated after transfection with Ad ASBTEB2. Ad ASBTEB2 treatment reduced I/M area ratios on day 7, 14, and 21 after injury by 45%, 50% and 53% respectively, whereas the Ad LacZ treatment did not significantly alter these ratios compared with control group. Conclusion： BTEB2 antisense RNA mediated by adenoviral vector inhibits proliferation of VSMCs and significantly reduces neointimal hyperplasia in the rat carotid balloon injury model. BTEB2 antisense RNA is a potential therapeutic approach to preventing neointimal formation after balloon injury.展开更多
Objective.The present study investigated the role of endogenous carbon monoxide(CO)in the pathogenesis of neointimal formation induced by balloon injury in rat. Method.Endothelial denudation ...Objective.The present study investigated the role of endogenous carbon monoxide(CO)in the pathogenesis of neointimal formation induced by balloon injury in rat. Method.Endothelial denudation of the left common carotid artery of rat was carried out by three passages of a Fogarty 2F balloon catheter.DNA,collagen and elastin contents of each intima media were estimated;and heme oxygenase(HO)activity and CO production in vascular smooth muscle cell(VSMC)were measured after administration of HO inhibitor. Result.Our data showed that neointima occurred in the rat on day 7 and day 21 after balloon injury,and at the same time HO activity and CO production in VSMC were markedly increased Administration of HO inhibitor,zinc deuteroporphyrin 2,4 bisglycol(ZnDPBG),could effectively inhibit HO activity and CO production,significantly enhance neointimal formation(aortic intima/media ratio were 21 4±1 8% vs 17 6±2 0%,P<0 05 on day 7;and 30 5±2 4% vs 23 0±2 2%,P<0 01 on day 21,respectively,compared with balloon alone group). Conclusion.We concluded that 1)inhibition of CO production may enhance neointimal formation induced by endothelial denudation,implying endogenous CO play an protective role in response to vascular injury,and 2)induction of HO activity may be applied clinically for preventing restenosis after angioplasty.展开更多
目的探讨糖尿病患者外周血内皮祖细胞(EPCs)体内再内皮化能力的变化。方法培养、鉴定EPCs;构建裸鼠颈动脉内膜损伤模型。分组:健康组移植健康人EPCs,糖尿病组移植糖尿病患者EPCs,PBS对照组移植PBS。显微镜下观察伊文斯蓝染色损伤内膜再...目的探讨糖尿病患者外周血内皮祖细胞(EPCs)体内再内皮化能力的变化。方法培养、鉴定EPCs;构建裸鼠颈动脉内膜损伤模型。分组:健康组移植健康人EPCs,糖尿病组移植糖尿病患者EPCs,PBS对照组移植PBS。显微镜下观察伊文斯蓝染色损伤内膜再内皮化的情况,HE染色观察损伤内膜与中膜的面积的厚度,借助Image-Pro Plus 5.0图像分析系统计算再内皮化率及内膜/中膜比值。结果糖尿病组内膜损伤修复面积(23.78±1.95)%小于健康组(35.93±4.37)%(P<0.05),内膜/中膜比值糖尿病组(74.50±6.80)%大于健康组(59.40±5.00)%(P<0.05)。结论糖尿病患者EPCs体内再内皮化及抑制内膜增生能力降低,可能是其血管内皮损伤及内皮修复能力下降的重要机制。展开更多
文摘Objective： To investigate the effects of basic transcriptional element binding protein-2 （BTEB2） antisense RNA on vascular smooth muscle cells （VSMCs） proliferation and the neointimal formation after carotid balloon injury in rats. Methods： The cultured VSMCs were transfected with an adenoviral vector containing BTEB2 antisense gene, Ad ASBTEB2. Effects of BTEB2 antisense RNA on the expression of BTEB2 were investigated by Western blot analysis. The cell cycle was analyzed using flow cytometry. Ad ASBTEB2, control adenoviral vector Ad. LacZ or PBS was transduced into the rat carotid artery after balloon injury. The expression of BTEB2 at 7, 14, and 21 d after gene transfer was detected by immunohistochemistry and neointima-to-media （I/M） area ratio at these time points was calculated. Resuits： The cell cycle was arrested in G0/G1 phase and the expression of BETB2 was downregulated after transfection with Ad ASBTEB2. Ad ASBTEB2 treatment reduced I/M area ratios on day 7, 14, and 21 after injury by 45%, 50% and 53% respectively, whereas the Ad LacZ treatment did not significantly alter these ratios compared with control group. Conclusion： BTEB2 antisense RNA mediated by adenoviral vector inhibits proliferation of VSMCs and significantly reduces neointimal hyperplasia in the rat carotid balloon injury model. BTEB2 antisense RNA is a potential therapeutic approach to preventing neointimal formation after balloon injury.
文摘Objective.The present study investigated the role of endogenous carbon monoxide(CO)in the pathogenesis of neointimal formation induced by balloon injury in rat. Method.Endothelial denudation of the left common carotid artery of rat was carried out by three passages of a Fogarty 2F balloon catheter.DNA,collagen and elastin contents of each intima media were estimated;and heme oxygenase(HO)activity and CO production in vascular smooth muscle cell(VSMC)were measured after administration of HO inhibitor. Result.Our data showed that neointima occurred in the rat on day 7 and day 21 after balloon injury,and at the same time HO activity and CO production in VSMC were markedly increased Administration of HO inhibitor,zinc deuteroporphyrin 2,4 bisglycol(ZnDPBG),could effectively inhibit HO activity and CO production,significantly enhance neointimal formation(aortic intima/media ratio were 21 4±1 8% vs 17 6±2 0%,P<0 05 on day 7;and 30 5±2 4% vs 23 0±2 2%,P<0 01 on day 21,respectively,compared with balloon alone group). Conclusion.We concluded that 1)inhibition of CO production may enhance neointimal formation induced by endothelial denudation,implying endogenous CO play an protective role in response to vascular injury,and 2)induction of HO activity may be applied clinically for preventing restenosis after angioplasty.
文摘目的探讨糖尿病患者外周血内皮祖细胞(EPCs)体内再内皮化能力的变化。方法培养、鉴定EPCs;构建裸鼠颈动脉内膜损伤模型。分组:健康组移植健康人EPCs,糖尿病组移植糖尿病患者EPCs,PBS对照组移植PBS。显微镜下观察伊文斯蓝染色损伤内膜再内皮化的情况,HE染色观察损伤内膜与中膜的面积的厚度,借助Image-Pro Plus 5.0图像分析系统计算再内皮化率及内膜/中膜比值。结果糖尿病组内膜损伤修复面积(23.78±1.95)%小于健康组(35.93±4.37)%(P<0.05),内膜/中膜比值糖尿病组(74.50±6.80)%大于健康组(59.40±5.00)%(P<0.05)。结论糖尿病患者EPCs体内再内皮化及抑制内膜增生能力降低,可能是其血管内皮损伤及内皮修复能力下降的重要机制。
