Schwann cells upregulate vascular endothelial growth factor secondary to chronic nerve compression injury.
To better understand the pathogenesis of chronic nerve compression injuries, we investigated the possibility that Schwann cell production of vascular endothelial growth factor (VEGF) is responsible for the increased vascularity and Schwann cell proliferation associated with chronic nerve injury. In situ hybridization was used to evaluate VEGF mRNA production with immunohistochemistry to further localize the production of VEGF and its receptor proteins in an animal model of chronic nerve compression injury. VEGF mRNA and protein expression increased within Schwann cells as early as 2 weeks after compression and peaked by 1 month with a subsequent marked increase in the number of blood vessels. Thus, chronic nerve compression injury induces Schwann cells to increase VEGF production, which may be responsible for changes in neural vasculature secondary to chronic nerve compression injury. With a better understanding of these nerve injuries, more effective treatments may be developed to help patients with these impairments.
Gupta
Ranjan
R
Peripheral Nerve Research Laboratory, Department of Orthopedic Surgery, Medical Sciences I, Room B120, University of California, Irvine, California 92697, USA. ranjang@uci.edu
Gray
Michael
M
Chao
Tom
T
Bear
David
D
Modafferi
Edward
E
Mozaffar
Tahseen
T
D000818:Animals; D002908:Chronic Disease; D008297:Male; D018919:Neovascularization, Physiologic / Q000502:physiology; D009408:Nerve Compression Syndromes / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012583:Schwann Cells / Q000737:chemistry / Q000378:metabolism*; D015854:Up-Regulation / Q000502:physiology*; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis / Q000096:biosynthesis*
D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat