Volume 272, Number 41, Issue of October 10, 1997 pp. 25636-25640
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Contractile Activity Stimulates the c-Jun NH₂-terminal Kinase Pathway in Rat Skeletal Muscle

(Received for publication, July 1, 1997, and in revised form, July 31, 1997)

From the Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02215

Contractile activity plays a critical role in the regulation of gene transcription in skeletal muscle, which in turn determines muscle functional capabilities. However, little is known about the molecular signaling mechanisms that convert contractile activity into gene regulatory responses in skeletal muscle. In the current study we determined the effects of contractile activity in vivo on the c-Jun NH₂-terminal kinase (JNK) pathway, a signaling cascade that has been implicated in the regulation of transcription. Electrical stimulation of the sciatic nerve to produce contractions in anaesthetized rats increased JNK activity by up to 7-fold above basal. Maximal enzyme activity occurred at 15 min of contraction and remained elevated at 60 min of contraction. The upstream activators of JNK, the mitogen-activated protein kinase kinase 4 and the mitogen-activated protein kinase kinase kinase 1 followed a similar time course of activation in response to contractile activity. In contrast, contraction induced a rapid and transient activation of the extracellular-regulated kinase pathway, indicating that the regulation of JNK signaling is distinct from that of extracellular-regulated kinase. The activation of the JNK signaling cascade was temporally associated with an increased expression of c-jun mRNA. These results demonstrate that contractile activity regulates JNK activity in skeletal muscle and suggest that activation of JNK may regulate contraction-induced gene expression in skeletal muscle.

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