Transient upregulation of Nerve injury induced protein 1 in the course of neuroinflammation in rat spinal cord injury

Abstract

Nerve injury-induced protein-1 (Ninjurin-1) is a cell surface protein that induces neurite growth in the rat sciatic nerve and plays an important role in the transmigration of macrophages to inflammatory lesions in the central nervous system (CNS). The present study evaluated Ninjurin-1 expression in rats following clip compression-induced spinal cord injury (SCI) to elucidate the involvement of this protein. Western blot analyses revealed that Ninjurin-1 was constitutively expressed in sham controls whereas, compared to the sham controls, Ninjurin-1 levels in SCI rats exhibited an upregulation until day 4 post-injury (PI) and then slightly declined thereafter. Immunohistochemistry analyses revealed weak Ninjurin-1 immunostaining in vascular endothelial cells, ependymal cells, and some glial cells in sham controls whereas SCI rats exhibited staining in macrophages/microglia and reactive astrocytes in the lesions of injured spinal cords. Taken together, these findings suggest that Ninjurin-1 was secreted by a variety of cells, including vascular endothelial cells, macrophages/microglia, and astrocytes that play pro-inflammatory roles immediately after injury and/or contribute to regeneration of the spinal cord following clip compression injury.