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1 Laboratory of Muscle Biology and Sarcopenia, Dept. Exercise Physiology, West Virginia University School of Medicine, Morgantown, WV, USA
* To whom correspondence should be addressed. E-mail: salway{at}hsc.wvu.edu.
The purpose of this study was to examine potential regulatory candidates activating apoptotic signaling in aging skeletal myocytes. Patagialis (PAT) muscle hypertrophy was induced by loading the left wing of young and aged quails for 14 days. The weight was then removed for either 7 or 14 days to induce muscle atrophy. The PAT from the contralateral wing served as the intra-animal control. Although nuclear Id2 protein content was not different between the unloaded and control muscles in all groups, cytoplasmic Id2 protein content of unloaded muscles was higher than contralateral control muscles after 7-days of unloading in young quails. Both nuclear and cytoplasmic p53 contents of the unloaded muscles were higher than control muscles after 7-days of unloading in young quails, whereas in aged quails the p53 and Id2 contents of the unloaded muscles were not significantly different from the intra-animal control muscles after 7- or 14-days of unloading. The p53 nuclear index estimated by immunofluorescent cytochemistry showed similar results as the immunoblots. Our double immunofluorescent staining suggested that presumably both existing myonuclei and activated satellite cell nuclei contributed to the increased number of p53-positive nuclei. Conversely, c-Myc protein content was not significantly different in unloaded muscles when compared to control muscles in both young adult and aged quails. Although CuZnSOD content was not different in unloaded and control muscles, MnSOD content in the unloaded muscle was elevated relative to the control muscle after 7-days of unloading in young quails, suggesting that unloading induced an oxidative disturbance in these PAT muscles. Moderate correlational relationships existed among Id2, p53, c-Myc, SOD, apoptosis regulatory factors, and TUNEL index. Our findings are in agreement with the hypothesis that Id2 and p53 are involved in the apoptotic responses during unloading-induced muscle atrophy following hypertrophy in young adult birds. Furthermore, our data suggest that there is an aging-dependent regulation of Id2 and p53 during unloading of previously hypertrophied muscles.
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