Conclusions
Mast cell degranulation and accumulation precede overload-induced angiogenesis, but mast cell activation is not critical to the angiogenic response following skeletal muscle overload.
Methods
Extensor digitorum longus muscle was overloaded through extirpation of the synergist muscle tibialis anterior. Muscles were removed after 1, 2, 4, 7 or 14 days, and mast cell density and degranulation were quantified by histology. The mast cell stabilizer, cromolyn, was administered acutely or chronically to test if mast cell degranulation contributes to overload-induced angiogenesis. Angiogenesis was determined by calculating capillary to muscle Fiber ratio; mast cell density and activation were quantified by histology, MMP-2 levels were assessed by gelatin zymography and VEGF protein levels were assessed by Western blotting.
Objective
To determine if mast cell activation in skeletal muscle contributes to overload-induced angiogenesis.
Results
Muscle overload increased mast cell degranulation and total mast cell number within 7 days. Mast cell stabilization with cromolyn attenuated degranulation but did not inhibit the increased mast cell density, MMP-2 activity, VEGF protein levels or the increase in capillary number following muscle overload. Conclusions: Mast cell degranulation and accumulation precede overload-induced angiogenesis, but mast cell activation is not critical to the angiogenic response following skeletal muscle overload.