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1 Division of Physiology, Department of Medicine, University of California, San Diego, La Jolla, CA, USA
2 Department of Molecular Oncology, Genentech, Incorporated, South San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: ktang{at}ucsd.edu.
Skeletal muscle angiogenesis is an important physiological adaptation to increased metabolic demand, possibly dependent on vascular endothelial growth factor (VEGF), the increased expression of which is a known early response to exercise. To test the hypothesis that VEGF is essential to muscle capillary maintenance, we evaluated the consequences of targeted skeletal muscle inhibition of VEGF expression in postnatal, cage-confined VEGFloxP (+/+) mice. To delete VEGF, cre recombinase expression was accomplished using direct intramuscular injection of a recombinant adeno-associated cre recombinase expressing viral vector. Four weeks post-infection, VEGF-inactivated regions revealed 64 percent decreases in capillary density and capillary to fiber ratio. Substantial apoptosis was also observed in VEGF depleted regions. There was no evidence of rescue at eight weeks, with a persistent 67 percent reduction in capillary to fiber ratio and a 69 percent decrease in capillary density. These data implicate VEGF as an essential survival factor for muscle capillarity and also demonstrate insufficient VEGF-dependent signaling leads to apoptosis in mouse skeletal muscle.
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