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Skeletal muscle remodeling in myofiber VEGF‐deficient exercise trained mice
Author(s) -
Delavar Hamid,
Rich Benjamin,
Wagner Peter D.,
Breen Ellen C.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.685.20
Subject(s) - skeletal muscle , angiogenesis , myocyte , endocrinology , medicine , ex vivo , gastrocnemius muscle , vimentin , chemistry , biology , immunohistochemistry , in vivo , microbiology and biotechnology
VEGF plays an essential role in regulating angiogenesis and clearance of apoptotic cells. A loss of skeletal myofiber expressed VEGF inhibits exercise‐induced angiogenesis. We hypothesized that skeletal myofiber VEGF deficient mice would increase fibroblast proliferation in hind limb muscles; especially following repeated bouts of exercise. Methods Using an HSA‐Cre‐ER T2 X VEGF LoxP (skmVEGF−/−) mouse model, VEGF levels are reduced by >;80% in skeletal muscles of adult mice compared to control littermates (WT). 8 week exercise trained (EX) and untrained (UT) mice were administered BrdU daily during the final week. Proliferating cells (BrdU+) and fibroblasts (vimentin+) were detected by confocal microscopy. Results Total BrdU+ cells/myofiber increased in UT and EX skmVEGF−/− mice compared to the WT‐UT and WT‐EX groups, respectively, in the plantaris (WT‐UT, 6%, skmVEGF−/−UT, 32%, WT‐EX, 37%, skmVEGF−/−EX, 47%) and gastrocnemius (WT‐UT, 2%, skmVEGF−/−UT, 43%, WT‐EX, 25%, skmVEGF−/−EX, 43%). Exercise training, alone, also increased BrdU incorporation in WT muscles. Gastrocnemius sections from exercise trained skmVEGF−/− mice displayed fibrotic foci containing numerous vimentin+/BrdU+ cells. These data suggest that VEGF may prevent muscle injury and fibrosis during exercise training.