Induction and maintenance of increased VEGF protein by chronic motor nerve stimulation in skeletal muscle

Brian H. Annex, Carol E. Torgan, Pengnian Lin, Doris A. Taylor, Michael A. Thompson, Kevin G. Peters, William E. Kraus

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


Vascular endothelial growth factor (VEGF) causes endothelial cell proliferation in vitro and angiogenesis in vivo. Glycolytic skeletal muscles have a lower capillary density than oxidative muscles but can increase their capillary density and convert to a more oxidative phenotype when subject to chronic motor nerve stimulation (CMNS). We used Western analysis and immunohistochemical techniques to examine VEGF protein in a rabbit CMNS model of glycolytic skeletal muscle and in muscles with innate glycolytic versus oxidative phenotypes. VEGF protein per gram of total protein was increased in stimulated vs. control muscles 2.9 ± 1.0, 3.6 ± 1.3, 3.1 ± 0.5, 4.4 ± 1.6, and 2.7 ± 0.3 times after 3 (n = 4), 5 (n = 2), 10 (n = 3), 21 (n = 3), and 56 (n = 2) days, respectively. VEGF protein was increased 3.1 ± 0.5 times (P < 0.005) before (3, 5, and 10 days) and remained elevated 3.7 ± 1.0 times (P < 0.05) after (21 and 56 days) the transition to an oxidative phenotype. By immunohistochemistry, VEGF protein was found primarily in the matrix between stimulated muscle fibers but not in the myocytes. In addition, VEGF protein was consistently lower in innate glycolytic compared with oxidative muscles. These findings suggest that VEGF plays a role in the alteration and maintenance of vascular density in mammalian skeletal muscles.

Original languageEnglish (US)
Pages (from-to)H860-H867
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number3 43-3
StatePublished - Mar 1998
Externally publishedYes


  • Angiogenesis
  • Endurance training
  • Exercise
  • Growth factor
  • Vascularity

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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