| Abstract No.: | A-C1080 |
| Country: | Canada |
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| Title: | EXPRESSION OF ALCAM IN THE SPINAL CORD AFTER CONTUSION INJURY |
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| Authors/Affiliations: | 1 Delphine Bouhy*; 1 Adriana Redesik; 1 Ruben Lopes-Vales; 1 Samuel David;
1 McGill Center for Neuroscience Research, Montreal, QC, Canada
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| Content: | Spinal cord injury (SCI) triggers a cascade of inflammatory responses at the site of injury within hours and lasts for several weeks. This inflammatory response causes further exacerbation of tissue damage and functional impairments, referred to as secondary damage. Activated leukocyte cell adhesion molecule (ALCAM), a 105kDa transmembrane glycoprotein of the Ig-superfamily, mediates leukocyte migration into the CNS in experimental autoimmune encephalitis (EAE), a widely used animal model of multiple sclerosis (MS). Blocking ALCAM reduces the migration of lymphocytes and monocytes across the BBB-endothelium in vitro.
Objective: The aim of this work is to characterize the expression patterns of ALCAM after SCI.
Materials and Methods: A computer-controlled contusion device was used to make well-defined moderate contusion lesions in the lower thoracic spinal cord of adult female C57BL/6 mice. Mice are sacrificed at various times post-injury. We assessed protein expression by Western blot, and cell type specific expression by immunofluorescence of ALCAM in the mouse spinal cord between 1 and 28 days after spinal cord contusion injury.
Results: We show that ALCAM expression is increased after injury. This increase can be detected 24 hours after SCI and remains elevated at 28 days post-injury. The time-course of ALCAM expression seems to parallel the invasion of macrophages into the spinal cord after injury. The histological analyses show that macrophages are the most important cellular type expressing ALCAM at the lesion site.
Conclusion: These results show that ALCAM is expressed by activated macrophages after SCI. This adhesion molecule may be an important candidate mediating the immune cell influx that induces secondary tissue damage after SCI. Its role will also be assessed in ALCAM null mice. |
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