.tgf-¦Â/myostatin Signal Pathway In The Weightlessness Muscle Atrophy And Its Mechanism

For the past few years, as the human exploration of space undertakings, human in aviation industry has made great achievement more and more frequently, and human also more and more frequently into space. In flight, microgravity will result in the occurrence of muscular atrophy weightlessness, thus seriously affecting the mission complete and return to the ground for astronauts, especially long-term health recovery space flight. But so far weightlessness, the formation mechanism of muscular atrophy is unclear, we need to continue to explore weightlessness, the formation mechanism of muscular atrophy in order to ensure the health of astronauts. Smad3 is an important intracellular mediator that transduces signals from TGF-β/Smad signaling pathway, which plays a pivotal role in the regulation of skeletal muscle growth and development. TGF-(3/myostatin signaling pathways has important function of regulation for skeletal growth, in this study, we use the wild type C57BL6 wild type rat as the research object, with tail suspension method in mice induced by the formation of weightlessness muscle atrophy, using PCR experiment method, the dynamic testing in mice tail suspension 0 days,5 days,10 days,20 days in its hind legs dorsal skeletal muscles that are soleus and gastrocnemius at the genetic level Myostatin express change; Analyzes in weightlessness muscular atrophy form process related muscular atrophy factors(Atroginl, MμRF1) and muscle fibre phenotype genes (MHC-I, MHC-II b) expression with the dynamic change and the correlation of myostatin expression; Explore whether Myostatin through regulation into muscle specific genes (MyoD and myogenin) expression participated in weightlessness muscular atrophy formation.This experimental results show that:1. Mice, which were in hindlimb unloading,myostatin mRNA expression increased in soleus and gastrocnemius, the different is myostatin mRNA expression increase fast in soleus, and there is a large extent of myostatin mRNA expression in soleus; 2. Mice, which were in hindlimb unloading, Atroginl mRNA and MμRF1 mRNA expression increased in soleus and gastrocnemius, this increase is similar, the only difference is Atroginl mRNA expression was increased quickly in two muscle tissue, amplitude big, among them slow soleus muscle in the amount Atroginl mRNA expression get to maximum after hindlimb unloading for 5 days in mice, Atroginl mRNA expression get to maximum in mixed muscle gastrocnemius expression in mice after hindlimb unloading for 10 days.3. Mice, which were in hindlimb unloading, MHC-I mRNA expression decrease in slow muscle soleus and mixed muscle gastrocnemius, but the amount of MHC-II b mRNA expression increased. That seems to imply that myostatin may regulate the conversion of muscle fiber, which is MHC-Ⅰ→MHC-Ⅱb.4. Mice, which were in hindlimb unloading, MyoD mRNA expression increas slowly in the slow muscle soleus and mixed gastrocnemius muscle, there are different add rules in slow muscle soleus and mixed muscle gastrocnemius, MyoD mRNA expression in reach maximum amount in the slow soleus after hindlimb unloading for 10 days. MyoD mRNA express quantity in gastrocnemius continuesed to increase to maximum gradually in mice fter hindlimb unloading for 20 days; myogenin mRNA expression decreased in soleus and gastrocnemius, and continued to decline in the soleus, and fell to minimum in soleus fter hindlimb unloading for 20 days. Myogenin mRNA expression fell to minimum in gastrocnemius after hindlimb unloading for 5 days,and this state remains unchanged after hindlimb unloading for 10 days and 20 days. Therefore, in this study we revealed for the first time in the tail suspension induction of weightlessness muscular atrophy formation process, the correlations for the dynamic change of myostatin expression and muscular atrophy genes and gene expression changes of muscle fiber phenotype, and discusses its participation in weightlessness forming mechanism of muscular atrophy.This study can be for weightlessness muscular atrophy effective against ways and drug targets to provide the basis for screening.