Gene therapy prolongs survival and restores function in murine and canine models of myotubular myopathy

Sci Transl Med. 2014 Jan 22;6(220):220ra10. doi: 10.1126/scitranslmed.3007523.

Abstract

Loss-of-function mutations in the myotubularin gene (MTM1) cause X-linked myotubular myopathy (XLMTM), a fatal, congenital pediatric disease that affects the entire skeletal musculature. Systemic administration of a single dose of a recombinant serotype 8 adeno-associated virus (AAV8) vector expressing murine myotubularin to Mtm1-deficient knockout mice at the onset or at late stages of the disease resulted in robust improvement in motor activity and contractile force, corrected muscle pathology, and prolonged survival throughout a 6-month study. Similarly, single-dose intravascular delivery of a canine AAV8-MTM1 vector in XLMTM dogs markedly improved severe muscle weakness and respiratory impairment, and prolonged life span to more than 1 year in the absence of toxicity or a humoral or cell-mediated immune response. These results demonstrate the therapeutic efficacy of AAV-mediated gene therapy for myotubular myopathy in small- and large-animal models, and provide proof of concept for future clinical trials in XLMTM patients.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Dependovirus / genetics
  • Diaphragm
  • Disease Models, Animal*
  • Dogs
  • Genetic Therapy / methods*
  • Genetic Vectors
  • Genotype
  • HEK293 Cells
  • Humans
  • Male
  • Mice
  • Mice, Knockout
  • Muscle Contraction
  • Muscle Weakness
  • Mutation
  • Myopathies, Structural, Congenital / genetics*
  • Myopathies, Structural, Congenital / mortality
  • Myopathies, Structural, Congenital / therapy*
  • Protein Tyrosine Phosphatases, Non-Receptor / genetics

Substances

  • Protein Tyrosine Phosphatases, Non-Receptor
  • myotubularin