Abstract
BackgroundSeveral muscle-specific microRNAs (myomiRs) are differentially expressed during cellular senescence. However, the role of dietary compounds on myomiRs remains elusive. This study aimed to elucidate the modulatory role of tocotrienol-rich fraction (TRF) on myomiRs and myogenic genes during differentiation of human myoblasts. Young and senescent human skeletal muscle myoblasts (HSMM) were treated with 50 μg/mL TRF for 24 h before and after inducing differentiation.ResultsThe fusion index and myotube surface area were higher (p < 0.05) on days 3 and 5 than that on day 1 of differentiation. Ageing reduced the differentiation rate, as observed by a decrease in both fusion index and myotube surface area in senescent cells (p < 0.05). Treatment with TRF significantly increased differentiation at days 1, 3 and 5 of young and senescent myoblasts. In senescent myoblasts, TRF increased the expression of miR-206 and miR-486 and decreased PTEN and PAX7 expression. However, the expression of IGF1R was upregulated during early differentiation and decreased at late differentiation when treated with TRF. In young myoblasts, TRF promoted differentiation by modulating the expression of miR-206, which resulted in the reduction of PAX7 expression and upregulation of IGF1R.ConclusionTRF can potentially promote myoblast differentiation by modulating the expression of myomiRs, which regulate the expression of myogenic genes.
Highlights
IntroductionSeveral muscle-specific microRNAs (myomiRs) are differentially expressed during cellular senescence
Several muscle-specific microRNAs are differentially expressed during cellular senescence
Senescent myoblasts exhibited different morphological features when treated with tocotrienol-rich fraction (TRF)
Summary
Several muscle-specific microRNAs (myomiRs) are differentially expressed during cellular senescence. Satellite cells, which are located between the basal lamina and sarcolemma, act as vital components of the skeletal muscle tissue as they possess regeneration capacity. These satellite cells are mitotically quiescent and arrested at the G0 phase. In response to stress, such as muscle injury or physiological change, satellite cells are activated and undergo myogenesis, which involves a series of processes [2]. These cells migrate to the damaged site and withdraw from the G0 phase to re-enter the cell cycle progression. The cells undergo proliferation, differentiation and subsequently fuse with the adjacent muscle fibre to form a new
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