Myostatin is a major factor involved in the regulation of skeletal muscle protein mass. High myostatin levels have been associated with an increase in myotube shrinkage. Enhanced myostatin expression is caused by pro-...Myostatin is a major factor involved in the regulation of skeletal muscle protein mass. High myostatin levels have been associated with an increase in myotube shrinkage. Enhanced myostatin expression is caused by pro-catabolic reactions involving compounds such as tumor necrosis factor (TNF)-α. The present study investigated the effects of agaro-oligosaccharides (AOSs) on hypercatabolism of myotubes exposed to TNF-α. C2C12 myotubes exposed to TNF-α in the presence or absence of AOSs. Myotube exposure to TNF-α resulted in a reduction in the amount of myosin heavy chain (MyHC) protein and a decrease in myotube diameter, which was associated with increased myostatin mRNA expression. AOSs prevented TNF-α-induced MyHC protein loss and restored normal myostatin mRNA levels, with agarobiose and agarotetraose effectively suppressing the hyperexpression of the mRNA. In addition, expression levels of the known myostatin inhibitors, latent transforming growth factor beta binding protein 3 (Ltbp3) and growth and differentiation factor-associated serum protein 1 (Gasp1) mRNAs, decreased more in TNF-α-induced myotubes than in the TNF-α-free control, possibly resulting in myostatin upregulation. However, AOSs restored nearly normal expression levels of Ltbp3 and Gasp1 mRNA, potentially suppressing myostatin expression. These findings suggest that AOSs could prevent myotube shrinkage induced by TNF-α.展开更多
文摘Myostatin is a major factor involved in the regulation of skeletal muscle protein mass. High myostatin levels have been associated with an increase in myotube shrinkage. Enhanced myostatin expression is caused by pro-catabolic reactions involving compounds such as tumor necrosis factor (TNF)-α. The present study investigated the effects of agaro-oligosaccharides (AOSs) on hypercatabolism of myotubes exposed to TNF-α. C2C12 myotubes exposed to TNF-α in the presence or absence of AOSs. Myotube exposure to TNF-α resulted in a reduction in the amount of myosin heavy chain (MyHC) protein and a decrease in myotube diameter, which was associated with increased myostatin mRNA expression. AOSs prevented TNF-α-induced MyHC protein loss and restored normal myostatin mRNA levels, with agarobiose and agarotetraose effectively suppressing the hyperexpression of the mRNA. In addition, expression levels of the known myostatin inhibitors, latent transforming growth factor beta binding protein 3 (Ltbp3) and growth and differentiation factor-associated serum protein 1 (Gasp1) mRNAs, decreased more in TNF-α-induced myotubes than in the TNF-α-free control, possibly resulting in myostatin upregulation. However, AOSs restored nearly normal expression levels of Ltbp3 and Gasp1 mRNA, potentially suppressing myostatin expression. These findings suggest that AOSs could prevent myotube shrinkage induced by TNF-α.
