Expression of shRNA from a tissue-specific pol II promoter is an effective and safe RNAi therapeutic

被引:157
作者
Giering, Jeffery C. [1 ,2 ]
Grimm, Dirk [1 ,2 ]
Storm, Theresa A. [1 ,2 ]
Kay, Mark A. [1 ,2 ]
机构
[1] Stanford Univ, Dept Pediat, Stanford, CA 94305 USA
[2] Stanford Univ, Dept Genet, Stanford, CA 94305 USA
关键词
D O I
10.1038/mt.2008.144
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 [微生物学]; 0836 [生物工程]; 090102 [作物遗传育种]; 100705 [微生物与生化药学];
摘要
It has been observed that overexpression of some short-hairpin RNAs (shRNAs) can induce acute cytotoxicity. This has raised concerns about the safety of using RNA interference (RNAi) technology as a potential therapeutic tool. We have sought to address this challenge of expression control by developing a mono-cistronic vector for the tissue-specific expression of an shRNA from a liver-derived polymerase (pol) II promoter. This new construct efficiently induces target silencing in hepatoma cells in vitro and in mouse livers in vivo. In order to demonstrate the therapeutic potential and improved safety of this approach, we selected an shRNA targeting the envelope surface antigen (sAg) of hepatitis B virus (HBV), which is among the most toxic when expressed from the commonly used U6 promoter. Packaging it as a double-stranded DNA into an adeno-associated virus (AAV) pseudotype 8 and delivering it at a high particle dose (1 x 10(12)) to HBV transgenic mice resulted in the stable reduction of serum sAg to 85% of starting levels, without any concomitant sign of liver damage. With this improved tolerability, the liver-specific pol II shRNA expression persisted for more than one year after the injection. We conclude that this pol II shRNA expression system combined with a potent delivery vector represents an effective alternative to either U6-based strategies or systems that achieve tissue specificity through the use of additional elements.
引用
收藏
页码:1630 / 1636
页数:7
相关论文
共 30 条
[1]
DEVEGVAR HEN, 1986, CELL, V47, P259
[2]
Probing tumor phenotypes using stable and regulated synthetic microRNA precursors [J].
Dickins, RA ;
Hemann, MT ;
Zilfou, JT ;
Simpson, DR ;
Ibarra, I ;
Hannon, GJ ;
Lowe, SW .
NATURE GENETICS, 2005, 37 (11) :1289-1295
[3]
RNA interference is mediated by 21-and 22-nucleotide RNAs [J].
Elbashir, SM ;
Lendeckel, W ;
Tuschl, T .
GENES & DEVELOPMENT, 2001, 15 (02) :188-200
[4]
Vector-based RNAi approaches for stable, inducible and genome-wide screens [J].
Fewell, Gwen D. ;
Schmitt, Karin .
DRUG DISCOVERY TODAY, 2006, 11 (21-22) :975-982
[5]
Gene silencing in alveolar type II cells using cell-specific promoter in vitro and in vivo -: art. no. e134 [J].
Gou, D ;
Narasaraju, T ;
Chintagari, NR ;
Jin, N ;
Wang, PC ;
Liu, L .
NUCLEIC ACIDS RESEARCH, 2004, 32 (17) :e134
[6]
Fatality in mice due to oversaturation of cellular microRNA/short hairpin RNA pathways [J].
Grimm, Dirk ;
Streetz, Konrad L. ;
Jopling, Catherine L. ;
Storm, Theresa A. ;
Pandey, Kusum ;
Davis, Corrine R. ;
Marion, Patricia ;
Salazar, Felix ;
Kay, Mark A. .
NATURE, 2006, 441 (7092) :537-541
[7]
Molecular basis for the recognition of primary microRNAs by the Drosha-DGCR8 complex [J].
Han, Jinju ;
Lee, Yoontae ;
Yeom, Kyu-Hyeon ;
Nam, Jin-Wu ;
Heo, Inha ;
Rhee, Je-Keun ;
Sohn, Sun Young ;
Cho, Yunje ;
Zhang, Byoung-Tak ;
Kim, V. Narry .
CELL, 2006, 125 (05) :887-901
[8]
FORMATION OF THE 3' END OF U1 SNRNA REQUIRES COMPATIBLE SNRNA PROMOTER ELEMENTS [J].
HERNANDEZ, N ;
WEINER, AM .
CELL, 1986, 47 (02) :249-258
[9]
Sequence-specific inhibition of small RNA function [J].
Hutvágner, G ;
Simard, MJ ;
Mello, CC ;
Zamore, PD .
PLOS BIOLOGY, 2004, 2 (04) :465-475
[10]
Khvorova A, 2003, CELL, V115, P209, DOI 10.1016/S0092-8674(03)00801-8