Increased expression of the close homolog of the adhesion molecule l1 in different cell types over time after rat spinal cord contusion

✍ Scribed by Junfang Wu; Philberta Y. Leung; April Sharp; Hyun Joon Lee; Jean R. Wrathall

• Publisher: John Wiley and Sons
• Year: 2011
• Tongue: English
• Weight: 927 KB
• Volume: 89
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.22598

✦ Synopsis

Abstract

The close homolog of the adhesion molecule L1 (CHL1) is important during CNS development, but a study with CHL1 knockout mice showed greater functional recovery after spinal cord injury (SCI) in its absence. We investigated CHL1 expression from 1 to 28 days after clinically relevant contusive SCI in Sprague‐Dawley rats. Western blot analysis showed that CHL1 expression was significantly up‐regulated at day 1 and further increased over 4 weeks after SCI. Immunohistochemistry of tissue sections showed that CHL1 in the intact spinal cord was expressed at low levels. By 1 day and through 4 weeks after SCI, CHL1 became highly expressed in NG2^+^ cells. Hypertrophic GFAP^+^ astrocytes also expressed CHL1 by 1 week after injury. The increase in CHL1 protein paralleled that of NG2 in the first week and GFAP between 1 and 4 weeks after injury. At 4 weeks, NG2^+^/CHL1^+^ cells and GFAP^+^/CHL1^+^ astrocytes were concentrated at the boundary between residual spinal cord tissue and the central lesion. NF200^+^ spinal cord axons approached but did not penetrate this boundary. In contrast, CHL1^+^ cells in the central lesion at 1 week and later colabeled with p75 and NG2 and were chronically associated with many NF200^+^ axons, presumably axons that had sprouted in association with CHL1^+^ Schwann cells infiltrating the cord after contusion. Thus, our study demonstrates up‐regulation of CHL1 in multiple cell types and locations in a rat model of contusion injury and suggests that this molecule may be involved both in inhibition of axonal regeneration and in recovery processes after SCI. © 2011 Wiley‐Liss, Inc.