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1 Departments of Biomedical Sciences, Physiology, and the Dalton Cardiovascular Institute, University of Missouri-Columbia, Columbia, MO, USA
* To whom correspondence should be addressed. E-mail: boothf{at}missouri.edu.
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 while 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 STAT3 peaked on recovery day 3 compared to day 0. GSK-3
phosphorylation was increased on the 6th and 15th recovery day. In addition, transient peaks in seven protein concentrations occurred at different times of recovery: STAT3, CaNA, CaNB, and 4E-BP1 protein concentrations peaked on the 3rd recovery day; p70S6k, STAT3, Akt, GSK3-, and on the 6th recovery day; and GSK3- on the 15th 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.
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