Vimentin Expression Following Mechanical Overload Induced Skeletal Muscle Hypertrophy Appears To Be Satellite Cell Dependent

Introduction: Vimentin (VIM) is an intermediate filament that plays a key role in development and regeneration of various tissue types. However, the expression of VIM during skeletal muscle hypertrophy has not been fully elucidated. Therefore, the purpose of this study was to determine the response of VIM following mechanical overload (MOV) with or without the presence of satellite cells. Methods: Pax7-DTA mice (age 4mo) were subjected to 3, 10 or 20 days of synergist ablation to induce overload of the plantaris muscle, time matched sham surgery mice served as controls. Following overload, the plantaris was removed and either sectioned for immunohistochemistry (IHC) or placed in Trizol for later RNA/protein isolation. Satellite cell depletion was confirmed via IHC to determine Pax7+ cells. VIM expression was also examined via RT-qPCR, western blotting, and IHC. Data were checked for normality via Shapiro-Wilks tests and two-way ANOVAs were performed with Tukey post-hoc tests. Results: In the Pax7-DTA mice, VIM expression revealed a significant Group, Time, and Group x time interaction (all P < 0.001). Further analysis revealed VIM expression was significantly upregulated in satellite cell intact mice after 3, 10, and 20 days of overload (all P < 0.001). VIM expression in the satellite cell depleted mice was non-responsive to 3 and 10 days of MOV (P = 0.964, and P = 0.984, respectively), however VIM expression following 20 days of MOV in satellite cell depleted mice was significantly increased compared to sham mice (P = 0.0047). Conclusion: VIM expression is responsive to hypertrophic stimuli and appears to be satellite cell dependent in the early stages of skeletal muscle hypertrophy. Funding was provided through discretionary funds for Michael Roberts at Auburn University. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.