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MUSCLE CELL BIOLOGY AND CELL MOTILITY
Departments of Biomedical Sciences and Physiology, and Dalton Cardiovascular Institute, University of Missouri, Columbia, Missouri 65211
Submitted 15 October 2002 ; accepted in final form 16 April 2003
Currently, the repertoire of cellular and molecular pathways that control
skeletal muscle atrophy and hypertrophy are not well defined. It is possible
that intracellular regulatory signaling pathways are active at different times
during the muscle hypertrophy process. The hypothesis of the given experiments
was that cellular signals related to protein translation would be active at
early time points of skeletal muscle regrowth, whereas transcriptional signals
would be active at later time points of skeletal muscle regrowth. The
phosphorylation status of p38 MAPK and JNK increased at the end of limb
immobilization but returned to control values at recovery day 3.
Transient increases in phosphorylation and in protein concentration occurred
during recovery of soleus muscle mass. Phosphorylation of Akt,
p70S6k, and signal transducer and activator of transcription 3
(STAT3) peaked on recovery day 3 compared with day 0.
Glycogen synthase kinase (GSK)-3
phosphorylation was increased on the
sixth and fifteenth recovery day. In addition, transient peaks in seven
protein concentrations occurred at different times of recovery: STAT3,
calcineurin A (CaNA), CaNB, and 4E-BP1 protein concentrations peaked on
the third recovery day; p70S6k, STAT3, Akt, and GSK3- peaked
on the sixth recovery day; and GSK3- peaked on the fifteenth recovery
day. The apexes of STAT3 and GSK3- protein concentrations remained
elevated for two recovery time points. Thus the time course of increase in
molecules of signaling pathways differed as the young rat soleus muscle regrew
from an atrophied state.
skeletal muscle; hypertrophy; rehabilitation; atrophy
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