Poster #068
Cross-talk between Annexin A2 and Dystrophin in skeletal muscle
Mentors: Alessandra Cecchini, PhD; Alessandra Sacco, PhD
Skeletal muscle represents 40% of body mass and allows movement. Upon injury, skeletal muscle regenerates; stem cells activate repairing the damaged tissue and restore its function. Two molecules involved in muscle regeneration are Dystrophin and Annexin-A2. Dystrophin protects the muscle from injury as it contracts. Annexin-A2 promotes membrane repair by preventing cell death. Dystrophin or Annexin-A2 deficiencies can respectively lead to neuromuscular diseases, e.g., Duchenne muscular dystrophies and worsening of muscular dystrophies. Because of their role during muscle regeneration, we studied the cross-talk between Annexin-A2 and Dystrophin in mouse muscle C2C12 cell line in proliferating and differentiating conditions, two crucial muscle repair processes. We used immunostaining to visualize the two proteins in-vitro. Our results show that while during proliferation Dystrophin is absent, upon differentiation it is upregulated and co-expressed with Annexin-A2. Deciphering this interaction will contribute to finding novel target pathways to improve skeletal muscle regeneration and disease.