Modelling Duchenne muscular dystrophy in MYOD1-converted urine-derived cells treated with 3-deazaneplanocin A hydrochloride.
Hotake TakizawaYuko HaraYoshitaka MizobeTaisuke OhnoSadafumi SuzukiKen InoueEri TakeshitaYuko Shimizu-MotohashiAkihiko IshiyamaMikio HoshinoHirofumi KomakiShin'ichi TakedaYoshitsugu AokiPublished in: Scientific reports (2019)
Duchenne muscular dystrophy (DMD) is a severe muscle disorder characterised by mutations in the DMD gene. Recently, we have completed a phase I study in Japan based on systemic administration of the morpholino antisense that is amenable to exon-53 skipping, successfully. However, to achieve the effective treatment of DMD, in vitro assays on patient muscle cells to screen drugs and patient eligibility before clinical trials are indispensable. Here, we report a novel MYOD1-converted, urine-derived cells (UDCs) as a novel DMD muscle cell model. We discovered that 3-deazaneplanocin A hydrochloride, a histone methyltransferase inhibitor, could significantly promote MYOGENIN expression and myotube differentiation. We also demonstrated that our system, based on UDCs from DMD patients, could be used successfully to evaluate exon-skipping drugs targeting DMD exons including 44, 50, 51, and 55. This new autologous UDC-based disease modelling could lead to the application of precision medicine for various muscle diseases.
Keyphrases
- duchenne muscular dystrophy
- induced apoptosis
- muscular dystrophy
- cell cycle arrest
- clinical trial
- endoplasmic reticulum stress
- end stage renal disease
- high throughput
- cell therapy
- newly diagnosed
- single cell
- poor prognosis
- gene expression
- stem cells
- randomized controlled trial
- bone marrow
- signaling pathway
- early onset
- cancer therapy
- cell proliferation
- peritoneal dialysis
- prognostic factors
- mesenchymal stem cells
- dna methylation
- study protocol
- patient reported outcomes
- double blind