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J Biol Chem, Vol. 275, Issue 2, 1457-1462, January 14, 2000
From the Growing evidence suggests that activation of
mitogen-activated protein kinase (MAPK) signal transduction mediates
changes in muscle gene expression in response to exercise.
Nevertheless, little is known about upstream or downstream regulation
of MAPK in response to muscle contraction. Here we show that ex
vivo muscle contraction stimulates extracellular signal-regulated
kinase 1 and 2 (ERK1/2), and p38MAPK phosphorylation.
Phosphorylation of ERK1/2 or p38MAPK was unaffected by
protein kinase C inhibition (GF109203X), suggesting that protein kinase
C is not involved in mediating contraction-induced MAPK signaling.
Contraction-stimulated phosphorylation of ERK1/2 and
p38MAPK was completely inhibited by pretreatment with
PD98059 (MAPK kinase inhibitor) and SB203580 (p38MAPK
inhibitor), respectively. Muscle contraction also activated MAPK downstream targets p90 ribosomal S6 kinase (p90Rsk),
MAPK-activated protein kinase 2 (MAPKAP-K2), and mitogen- and stress-activated protein kinase 1 (MSK1). Use of PD98059 or SB203580 revealed that stimulation of p90Rsk and MAPKAP-K2 most
closely reflects ERK and p38MAPK stimulation, respectively.
Stimulation of MSK1 in contracting skeletal muscle required the
activation of both ERK and p38MAPK. These data demonstrate
that muscle contraction, separate from systemic influence, activates
MAPK signaling. Furthermore, we are the first to show that contractile
activity stimulates MAPKAP-K2 and MSK1.
Effect of Contraction on Mitogen-activated Protein Kinase Signal
Transduction in Skeletal Muscle
INVOLVEMENT OF THE MITOGEN- AND STRESS-ACTIVATED PROTEIN KINASE
1*
,,,, and¶
Department of Clinical Physiology,
Karolinska Hospital and the Department of Physiology and Pharmacology,
Karolinska Institute, S-171 76 Stockholm and the § MRC
Protein Phosphorylation Unit, Department of Biochemistry, University of
Dundee, Dundee DD1 5EH, United Kingdom
*
This work was supported by Grants 12669, 12679, 9517, and
12211 from the Swedish Medical Research Council and by funds from the
Thurings Foundation, the Magnus Bergwalls Foundation, the Tore Nilsons
Foundation, the Novo Nordisk Foundation, the Marcus and Amalia
Wallenberg Foundation, the Harald and Greta Jeanssons Foundation, the
Swedish Diabetes Association, the Foundation of Scientific Studies of
Diabetology, and the Swedish Society for Medical Research.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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