Lu Ping, Wang Songhao, Cai Wenwei, Sheng Jing
Department of Geriatrics, Shanghai Ninth People's Hospital Affiliated Shanghai Jiao Tong University School of Medicine, China.
Front Biosci (Elite Ed). 2012 Jan 1;4(6):2022-8. doi: 10.2741/e522.
We investigated expression of TGF-beta 1/Smad3 after balloon injury in rat carotid arteries as well as the effects of blocking the TGF-beta 1/smad3 signaling pathway on carotid intimal hyperplasia. Rats were randomly divided into control group (C group) and injury group (S group). The latter were randomly divided into intervention group (antisense Smad3 adenovirus vector transfection after balloon injury) and blank control group (blank adenovirus vector transfection after balloon injury). Expression of Smad3 mRNA 1 d, 3 d, 1 week, 2 weeks and 1 month after injury and intima/media thickness ratios 1 d, 2 weeks and 3 months after injury in the intervention group were significantly lower than those in the injury group. Ki-67 expression in the intervention group was inhibited as shown in immunohistochemistry studies. These results demonstrated that antisense Smad3 adenovirus vector transfection can block TGF-beta 1/Smad3 signal transduction and thus inhibit intimal hyperplasia.
我们研究了大鼠颈动脉球囊损伤后TGF-β1/Smad3的表达情况，以及阻断TGF-β1/Smad3信号通路对颈动脉内膜增生的影响。大鼠被随机分为对照组（C组）和损伤组（S组）。损伤组又被随机分为干预组（球囊损伤后转染反义Smad3腺病毒载体）和空白对照组（球囊损伤后转染空白腺病毒载体）。干预组损伤后1天、3天、1周、2周和1个月时Smad3 mRNA的表达以及损伤后1天、2周和3个月时的内膜/中膜厚度比值均显著低于损伤组。免疫组化研究显示干预组Ki-67表达受到抑制。这些结果表明，反义Smad3腺病毒载体转染可阻断TGF-β1/Smad3信号转导，从而抑制内膜增生。
