Human miRNA miR-675 inhibits DUX4 expression and may be exploited as a potential treatment for Facioscapulohumeral muscular dystrophy.
Nizar Y SaadMustafa Al-KharsanSara E Garwick-CoppensGholamhossein Amini ChermahiniMadison A HarperAndrew PaloRyan L BoudreauScott Q HarperPublished in: Nature communications (2021)
Facioscapulohumeral muscular dystrophy (FSHD) is a potentially devastating myopathy caused by de-repression of the DUX4 gene in skeletal muscles. Effective therapies will likely involve DUX4 inhibition. RNA interference (RNAi) is one powerful approach to inhibit DUX4, and we previously described a RNAi gene therapy to achieve DUX4 silencing in FSHD cells and mice using engineered microRNAs. Here we report a strategy to direct RNAi against DUX4 using the natural microRNA miR-675, which is derived from the lncRNA H19. Human miR-675 inhibits DUX4 expression and associated outcomes in FSHD cell models. In addition, miR-675 delivery using gene therapy protects muscles from DUX4-associated death in mice. Finally, we show that three known miR-675-upregulating small molecules inhibit DUX4 and DUX4-activated FSHD biomarkers in FSHD patient-derived myotubes. To our knowledge, this is the first study demonstrating the use of small molecules to suppress a dominant disease gene using an RNAi mechanism.
Keyphrases
- muscular dystrophy
- long non coding rna
- cell proliferation
- gene therapy
- long noncoding rna
- poor prognosis
- endothelial cells
- duchenne muscular dystrophy
- healthcare
- skeletal muscle
- copy number
- gene expression
- induced pluripotent stem cells
- mesenchymal stem cells
- transcription factor
- replacement therapy
- pi k akt
- genome wide analysis