Department of Gene Therapy, Imperial College at the National Heart and Lung Institute, London SW3 6LR, UK.
Biomaterials. 2010 Mar;31(9):2665-72. doi: 10.1016/j.biomaterials.2009.12.005. Epub 2009 Dec 21.
We have assessed whether viscoelastic gels known to inhibit mucociliary clearance can increase lipid-mediated gene transfer. Methylcellulose or carboxymethylcellulose (0.25-1.5%) was mixed with complexes of the cationic lipid GL67A and plasmids encoding luciferase and perfused onto the nasal epithelium of mice. Survival after perfusion with 1% CMC or 1% MC was 90 and 100%, respectively. In contrast 1.5% CMC was uniformly lethal likely due to the viscous solution blocking the airways. Perfusion with 0.5% CMC containing lipid/DNA complexes reproducibly increased gene expression by approximately 3-fold (n=16, p<0.05). Given this benefit, likely related to increased duration of contact, we also assessed the effect of prolonging contact time of the liposome/DNA complexes by delivering our standard 80 microg DNA dose over either approximately 22 or 60 min of perfusion. This independently increased gene transfer by 6-fold (n=8, p<0.05) and could be further enhanced by the addition of 0.5% CMC, leading to an overall 25-fold enhancement (n=8, p<0.001) in gene expression. As a result of these interventions CFTR transgene mRNA transgene levels were increased several logs above background. Interestingly, this did not lead to correction of the ion transport defects in the nasal epithelium of cystic fibrosis mice nor for immunohistochemical quantification of CFTR expression. To assess if 0.5% CMC also increased gene transfer in the mouse lung, we used whole body nebulisation chambers. CMC was nebulised for 1h immediately before, or simultaneously with GL67A/pCIKLux. The former did not increase gene transfer, whereas co-administration significantly increased gene transfer by 4-fold (p<0.0001, n=18). This study suggests that contact time of non-viral gene transfer agents is a key factor for gene delivery, and suggests two methods which may be translatable for use in man.
我们评估了已知抑制黏液纤毛清除的黏弹性凝胶是否能增加脂质介导的基因转移。将甲基纤维素或羧甲基纤维素(0.25-1.5%)与阳离子脂质 GL67A 的复合物和编码荧光素酶的质粒混合,然后灌流到小鼠的鼻上皮。用 1%CMC 或 1%MC 灌流后的存活率分别为 90%和 100%。相比之下,1.5%CMC 由于粘性溶液堵塞气道而导致均匀致死。用含有脂质/DNA 复合物的 0.5%CMC 灌流可使基因表达增加约 3 倍(n=16,p<0.05)。鉴于这种益处,可能与接触时间延长有关,我们还评估了通过在大约 22 或 60 分钟的灌流期间输送我们的标准 80μgDNA 剂量来延长脂质体/DNA 复合物接触时间对基因转移的影响。这独立地将基因转移增加了 6 倍(n=8,p<0.05),并且通过添加 0.5%CMC 可以进一步增强,导致基因表达总体增强 25 倍(n=8,p<0.001)。由于这些干预,CFTR 转基因 mRNA 转基因水平比背景高出几个对数级。有趣的是,这并没有导致囊性纤维化小鼠鼻上皮的离子转运缺陷得到纠正,也没有导致 CFTR 表达的免疫组织化学定量得到纠正。为了评估 0.5%CMC 是否也能增加小鼠肺部的基因转移,我们使用了全身雾化室。在 GL67A/pCIKLux 之前或同时立即用 CMC 雾化 1 小时。前者没有增加基因转移,而同时给药则使基因转移增加了 4 倍(p<0.0001,n=18)。这项研究表明,非病毒基因传递剂的接触时间是基因传递的关键因素,并提出了两种可能适用于人类的方法。