Up-regulation of mitogen activated protein kinases in mdx skeletal muscle following chronic treadmill exercise.
Dystrophin, a product of the Duchenne muscular dystrophy gene, is a cytoskeletal protein of skeletal and cardiac muscle fibers. Dystrophin-deficient muscle fibers are abnormally vulnerable to mechanical stress including physical exercise, which is a powerful stimulator of mitogen-activated protein kinases (MAPKs). To examine how treadmill exercise affects MAPK family members in dystrophin-deficient skeletal muscle, we subjected both mdx mice, an animal model for Duchenne muscular dystrophy, and C57BL/10 mice to treadmill exercise and examined the phosphorylated protein levels of extracellular-signal regulated kinase (ERK1/2), p38 MAPK and c-Jun N terminal kinase 1 and 2 (JNK1 and JNK2) in the gastrocnemius muscle. Phosphorylation of ERK1/2, p38 MAPK and JNK2, but not JNK1, increased more in the muscles of exercise trained mdx mice than in muscles of trained C57BL/10 or untrained mdx mice. These results show that physical exercise aberrantly up-regulates the phosphorylated form of ERK1/2, p38 MAPK and JNK2 in dystrophin-deficient skeletal muscle and that their up-regulation might play a role in the degeneration and regeneration process of dystrophic features.
Nakamura
Akinori
A
Third Department of Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Yoshida
Kunihiro
K
Ueda
Hideho
H
Takeda
Shin'ichi
S
Ikeda
Shu-ichi
S
D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western; D003720:Densitometry; D016189:Dystrophin / Q000172:deficiency*; D051379:Mice; D008810:Mice, Inbred C57BL; D018101:Mice, Inbred mdx; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism*; D010766:Phosphorylation; D010805:Physical Conditioning, Animal; D015854:Up-Regulation
D016189:Dystrophin; D020928:Mitogen-Activated Protein Kinases