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Microcirculation. 2010 Oct;17(7):548-56. doi: 10.1111/j.1549-8719.2010.00049.x.

The angiogenic response to skeletal muscle overload is not dependent on mast cell activation.

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School of Kinesiology and Health Science, Muscle Health Research Centre, York University, Toronto, Ontario, Canada.



To determine if mast cell activation in skeletal muscle contributes to overload-induced angiogenesis.


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.


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.


Mast cell degranulation and accumulation precede overload-induced angiogenesis, but mast cell activation is not critical to the angiogenic response following skeletal muscle overload.

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