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Altered mitogen-activated protein kinase signaling in dystrophic (mdx) muscle

Gayle M Smythe1, Jade K Forwood

  • 1School of Community Health, Charles Sturt University, P.O. Box 789, Albury, NSW, 2640, Australia. gsmythe@csu.edu.au

Muscle & Nerve
|August 22, 2012
PubMed
Abstract

Insights

Duchenne muscular dystrophy (DMD) involves altered mitogen-activated protein (MAP) kinase signaling, making muscle cells more vulnerable to stress. Targeting these MAP kinase pathways could offer new treatments for DMD.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Biochemistry

Background:

  • Duchenne muscular dystrophy (DMD) is caused by dystrophin deficiency, leading to muscle cell susceptibility to stress.
  • Altered pro-survival signaling pathways are implicated in dystrophic myotubes, but the role of mitogen-activated protein (MAP) kinases remains unexplored.

Purpose of the Study:

  • To investigate the role of MAP kinase signaling pathways in the context of Duchenne muscular dystrophy.
  • To examine the phosphorylation patterns of key MAP kinase proteins in dystrophic muscle cells and tissue.

Main Methods:

  • Cultured myotubes from dystrophic (mdx) and wild-type mice were subjected to oxidative stress.
  • Phosphorylation patterns of key MAP kinase proteins were analyzed in vitro and in muscle tissue samples in vivo.

Main Results:

  • Dystrophic myotubes exhibited increased susceptibility to oxidant-induced cell death compared to wild-type.
  • This heightened susceptibility correlated with late c-Jun N-terminal kinase (JNK) phosphorylation and sustained p38 MAP kinase phosphorylation in mdx myotubes.
  • Altered phosphorylation levels of JNK and extracellular signal-regulated kinase 1/2 (ERK1/2) were observed in mdx muscle tissue.

Conclusions:

  • Significant alterations in MAP kinase protein phosphorylation were identified in dystrophic muscle, both in vitro and in vivo.
  • These findings suggest that MAP kinase signaling pathways represent potential novel pharmacological targets for therapeutic intervention in DMD.

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