报告内容摘要：

Little is known regarding the interplays between the mechanical and molecular bases for tissue homeostasis and pathogenesis. We recently used C2C12 myoblasts to investigate the role of PPARs and their transcriptional activity during myotube formation. The role of mechanical stretch during myogenesis was also explored by applying cyclic stretch to the differentiating C2C12 myoblasts with 10% strain deformation at 1 Hz. The myogenesis of C2C12 was induced by culting on myogenesis medium (MM) to facilitate myotube formation with increased myosin heavy chain and α-smooth muscle actin (α-SMA) protein expression. The PPARγ protein and PPAR response element (PPRE) promoter activity decreased during MM induction. Cyclic stretch further facilitated the myogenesis in MM with increased α-SMA and decreased PPARγ protein expression and inhibited PPRE promoter activity. In addition, the side effect of PPARγ agonist (such as TZD) for inhibiting the myogenesis and restored the PPRE promoter activity can rescued by cyclic stretch. On the other hand, the mismatch of mechanical loading can cause tissue pathogenesis. Using venous-arterial transition of shear stress as an animal model, we discovered the shear stress overload induced the molecular cascades for autophagy and apoptosis in venous endothelial cells (ECs) to cause neointimal hyperplasia. We elucidated the stenosis initiation using a high-frequency ultrasonic (HFU) echogenicity platform and estimated the endothelium yield stress from von-Mises stress computation to predict the damage locations in living rats over time. Therefore, these results highlighted the importance of proper mechanical stimuli for the homeostasis and pathogenesis in musculoskeletal and cardiovascular system.
 
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