Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Hum Gene Ther. 2011 Dec;22(12):1483-97. doi: 10.1089/hum.2010.234. Epub 2011 Oct 4.
RNA interference (RNAi) has become the cornerstone technology for studying gene function in mammalian cells. In addition, it is a promising therapeutic treatment for multiple human diseases. Virus-mediated constitutive expression of short hairpin RNA (shRNA) has the potential to provide a permanent source of silencing molecules to tissues, and it is being devised as a strategy for the treatment of liver conditions such as hepatitis B and hepatitis C virus infection. Unintended interaction between silencing molecules and cellular components, leading to toxic effects, has been described in vitro. Despite the enormous interest in using the RNAi technology for in vivo applications, little is known about the safety of constitutively expressing shRNA for multiple weeks. Here we report the effects of in vivo shRNA expression, using helper-dependent adenoviral vectors. We show that gene-specific knockdown is maintained for at least 6 weeks after injection of 1 × 10(11) viral particles. Nonetheless, accumulation of mature shRNA molecules was observed up to weeks 3 and 4, and then declined gradually, suggesting the buildup of mature shRNA molecules induced cell death with concomitant loss of viral DNA and shRNA expression. No evidence of well-characterized innate immunity activation (such as interferon production) or saturation of the exportin-5 pathway was observed. Overall, our data suggest constitutive expression of shRNA results in accumulation of mature shRNA molecules, inducing cellular toxicity at late time points, despite the presence of gene silencing.
RNA 干扰 (RNAi) 已成为研究哺乳动物细胞中基因功能的基石技术。此外,它是治疗多种人类疾病的有前途的治疗方法。病毒介导的短发夹 RNA (shRNA) 的组成型表达有可能为组织提供沉默分子的永久来源,并且正在被设计为治疗乙型肝炎和丙型肝炎病毒感染等肝脏疾病的策略。体外已经描述了沉默分子与细胞成分之间的意外相互作用,导致毒性作用。尽管人们对将 RNAi 技术用于体内应用非常感兴趣,但对于连续数周表达 shRNA 的安全性知之甚少。在这里,我们报告了使用辅助依赖性腺病毒载体进行体内 shRNA 表达的效果。我们表明,在注射 1×10(11)个病毒颗粒后,至少在 6 周内保持基因特异性敲低。尽管如此,在第 3 和第 4 周观察到成熟 shRNA 分子的积累,然后逐渐减少,这表明成熟 shRNA 分子的积累诱导细胞死亡,同时伴随着病毒 DNA 和 shRNA 表达的丧失。没有观察到特征明确的先天免疫激活(例如干扰素产生)或输出蛋白 5 途径的饱和的证据。总体而言,我们的数据表明,尽管存在基因沉默,但 shRNA 的组成型表达会导致成熟 shRNA 分子的积累,从而在后期引起细胞毒性。