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JNK p46 is activated when skeletal muscle contracts in response to electrical stimulation of the sciatic never in rat
Author(s) -
Zhou YanWen,
Jiang Daifeng,
Jarrett Harry W.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a269-d
Subject(s) - skeletal muscle , duchenne muscular dystrophy , laminin , dystrophin , stimulation , microbiology and biotechnology , chemistry , signal transduction , neuromuscular junction , endocrinology , medicine , contraction (grammar) , muscular dystrophy , muscle contraction , biology , neuroscience , extracellular matrix
In a previously study ( J. Biol., Chem . 278 : –39295, 2003), we described a putative signaling pathway where, when laminin binds the dystrophin glycoprotein complex (DGC) of skeletal muscle, signaling occurs through dystroglycan‐syntrophin‐Rac1 and JNKp46 is activated. Since laminin is tightly bound in vivo , we investigated whether strain on the laminin‐DGC linkage during contraction is what stimulates this signaling pathway in vivo . When the gastrocnemius is contracted by electric stimulation of the sciatic nerve, Rac1 is activated relative to the unstimulated contralateral control muscle and Rac1 co‐localizes with β‐dystroglycan. Thus, muscle contraction caused a similar effect as laminin addition in vitro . The complete signaling pathway must function since contraction also caused the activation of JNKp46, a JNK1 isoform, and DNA‐binding by several downstream transcription factors is also affected by either contraction or laminin‐binding. These data would suggest that when this complex is defective in the mdx mouse model for Duchenne muscular dystrophy, less active JNKp46 should be found and this is the case. Interestingly, mdx mouse muscle actually contains greater amounts of JNKp46 but very little of it is activated and much less than in equal amounts of the control, normal muscle. (This work was supported by NIH AR051440 and by the Muscular Dystrophy Association, grant #3789)