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The Angiogenic Response to Skeletal Muscle Overload is not Dependent on Mast Cell Activation
Author(s) -
DOYLE JENNIFER L.,
HAAS TARA L.
Publication year - 2010
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/j.1549-8719.2010.00049.x
Subject(s) - degranulation , mast cell , angiogenesis , skeletal muscle , medicine , cell , chemistry , endocrinology , biology , immunology , biochemistry , receptor
Please cite this paper as: Doyle and Haas (2010). The Angiogenic Response to Skeletal Muscle Overload is not Dependent on Mast Cell Activation. Microcirculation 17(7) , 548–556. Abstract Objective: To determine if mast cell activation in skeletal muscle contributes to overload‐induced angiogenesis. 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. 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.