title: Increased expression of the close homolog of the adhesion molecule L1 in different cell types over time after rat spinal cord contusion.
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.
authors.affiliation: Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA. jwu@anes.umm.edu
authors.forename: Junfang
authors.initials: J
authors.lastname: Wu
authors.forename: Philberta Y
authors.initials: PY
authors.lastname: Leung
authors.forename: April
authors.initials: A
authors.lastname: Sharp
authors.forename: Hyun Joon
authors.initials: HJ
authors.lastname: Lee
authors.forename: Jean R
authors.initials: JR
authors.lastname: Wrathall
mesh_terms: D000818:Animals; D001369:Axons / Q000473:pathology; D015815:Cell Adhesion Molecules / Q000096:biosynthesis* / Q000235:genetics; D019062:Cell Adhesion Molecules, Neuron-Glia / Q000096:biosynthesis* / Q000235:genetics / Q000502:physiology; D002478:Cells, Cultured; D004195:Disease Models, Animal; D005260:Female; D009416:Nerve Regeneration / Q000235:genetics / Q000502:physiology*; D009433:Neural Inhibition / Q000235:genetics / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000235:genetics / Q000502:physiology*; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D013997:Time Factors
chemical_list: C560119:CHL1 protein, rat; D015815:Cell Adhesion Molecules; D019062:Cell Adhesion Molecules, Neuron-Glia