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Schwann cells upregulate vascular endothelial growth factor secondary to chronic nerve compression injury
Author(s) -
Gupta Ranjan,
Gray Michael,
Chao Tom,
Bear David,
Modafferi Edward,
Mozaffar Tahseen
Publication year - 2005
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.20272
Subject(s) - vascular endothelial growth factor , medicine , nerve injury , nerve growth factor , pathology , in situ hybridization , nerve guidance conduit , angiogenesis , downregulation and upregulation , schwann cell , vascularity , pathogenesis , anatomy , biology , receptor , anesthesia , messenger rna , vegf receptors , peripheral nerve , biochemistry , gene
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. Muscle Nerve, 2005