Skeletal Muscle Autophagy

Abstract: 

Skeletal Muscle Autophagy

Prolonged inactivity results in skeletal muscle atrophy including increased reactive oxygen species (ROS) generation, inflammation, protein degradation, and weight loss. Over-expression of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) has been shown to increase mitochondria biogenesis and reduce oxidative stress and inflammation. However, in the process of investigating the effect of various atrophy-inducing stimuli on signal transduction pathways in skeletal muscle, few studies have shown the role of PGC-1α on mitochondrial biogenesis, antioxidant defense, and/or inflammatory response.

These researchers want to to elucidate the effect of hind-limb banding-induced immobilization (IM) and remobilization (RM) on mitochondrial adaptation in mouse skeletal muscle and to investigate the role of PGC-1α pathways in the cellular and molecular changes occurring following muscle IM and during recovery. They hypothesize that PGC-1α over-expression would promote mitochondrial biogenesis and thus ameliorate muscle metabolic and biochemical adaptation following disuse atrophy. In addition, mice hindlime immobilization induces decreased mitochondrial biogenesis and increased inflammatory responses, which may cause decreased mitochondrial renewal. Thus, the researchers are screening mitochondrial gene expressions using the NGS system. The project may also involve gene expression profiling on RNA extracted from the tibialis anterior muscle, which can be performed using the Galaxy software.

Group name: 
jil