Nerve Root Compression Increases Spinal Astrocytic Vimentin in Parallel With Sustained Pain and Endothelial Vimentin in Association With Spinal Vascular Reestablishment.
METHODS
Temporal immunohistochemistry analysis of spinal cord tissue from a rat model of cervical radiculopathy.


OBJECTIVE
The goal was to measure spinal endothelial and astrocytic vimentin expression after a painful nerve root compression to define spinal cellular expression of vimentin in the context of pain.


BACKGROUND
The intermediate filament, vimentin, is expressed in a variety of cell types in the spinal cord and is modulated in response to neural pathologies. Early after nerve root compression spinal astrocytes become activated and blood-spinal cord barrier (BSCB) breakdown occurs in parallel with development of pain-related behaviors; these spinal responses remain activated as does the presence of pain. In addition to vimentin, glial fibrillary acidic protein (GFAP) expression is a hallmark of astrocyte activation. In contrast, vascular endothelial cells down-regulate vimentin expression in parallel with vascular breakdown. It is not known whether spinal astrocytes and endothelial cells modulate their expression of vimentin in response to a painful neural injury.


METHODS
Mechanical hyperalgesia was measured and spinal cord tissue was harvested at days 1 and 7 after a unilateral nerve root compression in rats. Vimentin was coimmunolabeled with GFAP to label astrocytes and von Willebrand factor (VWF) for endothelial cells in the spinal cord on the side of injury.


RESULTS
Spinal astrocytic vimentin increases by day 7 after nerve root compression, corresponding to when mechanical hyperalgesia is maintained. Spinal endothelial vimentin increases as early as day 1 after a painful compression and is even more robust at day 7.


CONCLUSIONS
The delayed elevation in spinal astrocytic vimentin corresponding to sustained mechanical hyperalgesia supports its having a relationship with pain maintenance. Further, since BSCB integrity has been shown to be reestablished by day 7 after a painful compression, endothelial expressed vimentin may help to fortify spinal vasculature contributing to BSCB stability.


METHODS
N/A.
Department of Bioengineering, University of Pennsylvania, Philadelphia, PA.
Jenell R
JR
Smith
Department of Bioengineering, University of Pennsylvania, Philadelphia, PA.
Jasmine
J
Lee
Department of Bioengineering, University of Pennsylvania, Philadelphia, PA.|Department of Neurosurgery, University of Pennsylvania, Philadelphia, PA.
Beth A
BA
Winkelstein
D000818:Animals; D001253:Astrocytes / Q000378:metabolism* / Q000473:pathology; D002574:Cervical Vertebrae; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000473:pathology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006930:Hyperalgesia / Q000378:metabolism / Q000473:pathology; D008297:Male; D009408:Nerve Compression Syndromes / Q000378:metabolism / Q000473:pathology; D010146:Pain / Q000378:metabolism* / Q000473:pathology; D011843:Radiculopathy / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013126:Spinal Nerve Roots / Q000378:metabolism* / Q000473:pathology; D014746:Vimentin / Q000378:metabolism*
D005904:Glial Fibrillary Acidic Protein; D014746:Vimentin