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Abstract Details

Comparing Acute Skeletal Muscle Repair in Aged and Young Mice
Neuromuscular and Clinical Neurophysiology (EMG)
P4 - Poster Session 4 (8:00 AM-9:00 AM)
11-005
The purpose of this project was to identify the reasoning behind the decreased rate and efficacy of the body’s ability to repair and regenerate skeletal muscle when of older age, which in turn negatively affects the healing process and to determine the presence of Sarcopenia, an age-related loss of muscle size.
In time, biological processes slow down, and cells lose their ability to function properly or as actively as they once did, increasing the chances of cellular damage. With aging, the regenerative process's ability to repair deteriorates, indicating the genes involved with the aforementioned healing process are possibly disrupted or less expressed.

15 male mice (C57BL/6J breed) in each age category, 80 and 10 weeks old. Each receive chemical induced trauma to their right quadricep through barium chloride injection. Quadricep tissue is extracted and collected at five timepoints (day zero, one, three, seven, and fourteen), notable within the regenerative and repair process. RNA is extracted, purified from the tissue, then qRT-PCR is conducted, a method that quantifies changes in gene expression, allowing for the differentiation between the two groups. Using ImageJ, histopathological images of uninjured myofibers are taken to obtain the values of cross-sectional areas per myofiber. 

The results did not show meaningful distinction between the two age groups, rejecting the hypothesis set, that the expression of inflammatory, myogenic, and/or extracellular genes would be altered for the aged mice. Separately, the presence of sarcopenia was determined through cross-sectional examination of myofibers, showing elders suffering from a decrease in myofiber size.

The sample size may have negatively affected the results because it was too small to accurately represent the whole. Even so, myogenic genes are still shown to have been expressed less in aged mice, possibly indicating that these genes may play a more important role in the regenerative process. 

Authors/Disclosures

PRESENTER
No disclosure on file