Activation of Embryonic Intermediate Filaments Contributes to Glial Scar Formation after Spinal Cord Injury in Rats

• Published in: Journal of veterinary science (Suwŏn-si, Korea) Vol. 4; no. 2; pp. 109 - 112
• Main Authors: Kim, Do-hyun, Heo, Seung-dam, Ahn, Mee-jung, Sim, Ki-bum, Shin, Tae-kyun
• Format: Journal Article
• Language: English
• Published: Korea (South) 대한수의학회 2003
• Subjects: Animals; Cicatrix - pathology; Glial Fibrillary Acidic Protein - analysis; Immunohistochemistry; Intermediate Filament Proteins - analysis; Intermediate Filaments - physiology; Nerve Tissue Proteins; Nestin; Neuroglia - pathology; Rats; Rats, Sprague-Dawley; Spinal Cord Injuries - pathology; Vimentin - analysis; spinal cord injury; vimentin; nestin
• ISSN: 1229-845X; 1976-555X
• DOI: 10.4142/jvs.2003.4.2.109

The expression of two intermediate filaments, nestin and vimentin, was studied in spinal cord injury (SCI) to elucidate their roles in the formation of glial scars. Rats were sacrificed 1, 4, and 7 days after induction of compression injury of the spinal cord using an aneurysm clip. The affected spinal cords were studied using antibodies against nestin and vimentin intermediate filaments. One day after spinal cord injury, some clusters of nestin-positive vessels were detected in the center of the injury, but few were seen in other cell types. Vimentin immunostaining was detected in some glial cells in the center and its level of immunoreactivity was enhanced in the ependymal cells of the central canal. On days 4 and 7 after spinal cord injury, astrocytes and some ependymal cells in the central canal were stained positively for nestin and increased expression of nestin was observed in vessels. Vimentin was detected in some macrophages and astrocytes in the lesions. Nestin was co-localized with glial fibrillary acidic protein in some glial cells in SCI. These findings imply that spinal cord cells in adult animals have embryonic capacity, and these cells are activated after injury, which in turn contributes to repair of spinal cord injury through formation of a glial scar.