跨膜蛋白66过表达减轻大鼠颈动脉球囊损伤后内膜增生

摘要

Objective To clarify the role of transmembrane protein 66(TMEM66) in intima proliferation of carotid artery induced by balloon injury in rats.Methods SD rats were randomly divided into three groups (n=10), including control group, the left carotid artery balloon injury group and injury group added with lentiviruses, respectively.Accordingly, the intima proliferation of carotid artery were detected by H/E staining;the expressions of TMEM66 in carotid artery injuried by balloon were determined by Western blot,q-PCR and immunohistochemistry, and the migration and proliferation of VSMCs were measured by scratch test and CCK8 respectively.Results Compared with control group, the expression of TMEM66 in carotid artery was obviously decreased after balloon injury (P<0.05).Most importantly, the intima proliferation of carotid artery was significantly reversed by overexpression of TMEM66 via specific lentiviruses (P<0.05).Conclusions TMEM66 is able to attenuate the intima proliferation of carotid artery after balloon injury.It could be that upregulation of TMEM66 can alleviate the migration and proliferation of VSMCs by PDGF.%目的研究跨膜蛋白66(TMEM66)在大鼠颈动脉球囊损伤后内膜增生中的作用.方法将SD大鼠随机分为对照组,左侧颈动脉球囊损伤组和TMEM66过表达组(n=10).HE染色检测各组血管内膜增生情况.Western blot、q-PCR及IHC分别检测颈动脉血管中TMEM66的表达.CCK8和划痕实验分别检测TMEM66过表达后原代培养血管平滑肌细胞(VSMC)的增殖和迁移.结果颈动脉球囊损伤血管中TMEM66的表达量较对照组显著下降(P<0.05).球囊损伤后血管内膜明显增生,慢病毒特异性转染TMEM66过表达可显著逆转血管内膜增生(P<0.05).上调TMEM66能够改善PDGF所诱导的VSMC增殖和迁移(P<0.05).结论TMEM66可以改善大鼠颈动脉球囊损伤后内膜增生.