We used the model of 14 days Hindlimb Unloading (HU) in mice to study the mechanisms underlying disuse induced skeletal muscle atrophy by proteomic analysis.

We analyzed soleus and gastrocnemius as an example of a slow and a fast hindlimb muscle respectively. In soleus, a marked slow to fast shift of MHCs isoforms and a significant decrease of CSA of both slow and fast fibres was found following HU. The proteome map of soleus of control and HU mice was defined and a differential proteome analysis was performed. More than 800 protein spots on each gel were detected by fluorescent staining. Only a little percentage of detected spots were differentially expressed in HU mice in comparison with control animals. Most of the differentially expressed spots were implicated in oxidative stress (Hsp, SOD1, PRDX6, CAH III). Data showed an up-regulation of SOD1 and a down-regulation of other defence systems: Hsp, PRDX6, CAH III, suggesting the presence of oxidative stress in hindlimb suspended mice and a damage of defence system against oxidative stress.

Gastrocnemius muscle showed a lower degree of HU induced atrophy and few changes in protein pattern. SOD1, PRDX6, CAH III were up-regulated, whereas no changes were found in HSPs. Since data target the oxidative stress as one of the main mechanisms underlining disuse induced atrophy, the HU14 mice were treated with an antioxidant (30 mg/kg/day Trolox) to counteract the effects of oxidative damage and differential proteome maps of soleus and gastrocnemius muscles were obtained.