Neuromuscular Disorders, Biocruces Bizkaia Health Research Institute, 48903, Barakaldo, Bizkaia, Spain.
Osakidetza Basque Health Service, Bilbao-Basurto Integrated Health Organisation, Basurto University Hospital, Clinical Laboratory Service, Bilbao, Spain.
Sci Rep. 2021 Sep 14;11(1):18188. doi: 10.1038/s41598-021-97730-5.
Gene editing methods are an attractive therapeutic option for Duchenne muscular dystrophy, and they have an immediate application in the generation of research models. To generate myoblast cultures that could be useful in in vitro drug screening, we have optimised a CRISPR/Cas9 gene edition protocol. We have successfully used it in wild type immortalised myoblasts to delete exon 52 of the dystrophin gene, modelling a common Duchenne muscular dystrophy mutation; and in patient's immortalised cultures we have deleted an inhibitory microRNA target region of the utrophin UTR, leading to utrophin upregulation. We have characterised these cultures by demonstrating, respectively, inhibition of dystrophin expression and overexpression of utrophin, and evaluating the expression of myogenic factors (Myf5 and MyH3) and components of the dystrophin associated glycoprotein complex (α-sarcoglycan and β-dystroglycan). To demonstrate their use in the assessment of DMD treatments, we have performed exon skipping on the DMDΔ52-Model and have used the unedited DMD cultures/ DMD-UTRN-Model combo to assess utrophin overexpression after drug treatment. While the practical use of DMDΔ52-Model is limited to the validation to our gene editing protocol, DMD-UTRN-Model presents a possible therapeutic gene edition target as well as a useful positive control in the screening of utrophin overexpression drugs.
基因编辑方法是治疗杜氏肌营养不良症的一种有吸引力的治疗选择,并且它们可以立即应用于研究模型的生成。为了生成可用于体外药物筛选的成肌细胞培养物,我们优化了 CRISPR/Cas9 基因编辑方案。我们已经成功地将其用于野生型永生化成肌细胞,以删除肌营养不良蛋白基因的外显子 52,模拟常见的杜氏肌营养不良症突变;并且在患者的永生化培养物中,我们删除了肌联蛋白 UTR 的抑制性 microRNA 靶区,导致肌联蛋白上调。我们通过分别证明抑制肌营养不良蛋白的表达和过表达肌联蛋白,以及评估肌生成因子(Myf5 和 MyH3)和肌营养不良蛋白相关糖蛋白复合物的组成部分(α- sarcoglycan 和β-dystroglycan)来对这些培养物进行了特征描述。为了证明它们在评估 DMD 治疗中的用途,我们对 DMDΔ52-Model 进行了外显子跳跃,并使用未经编辑的 DMD 培养物/ DMD-UTRN-Model 组合在药物治疗后评估肌联蛋白的过表达。虽然 DMDΔ52-Model 的实际用途仅限于我们的基因编辑方案的验证,但 DMD-UTRN-Model 不仅是一种潜在的治疗性基因编辑靶标,而且在筛选肌联蛋白过表达药物时也是一种有用的阳性对照。