Adhesion molecules close homolog of L1 and tenascin-C affect blood-spinal cord barrier repair.

Abstract

Mice deficient in the recognition molecules, close homolog of L1 (CHL1) and tenascin-C, show improved and reduced functional recovery, respectively, after spinal cord injury compared with wild-type littermates. In this study, we addressed the question whether the differential functional outcome was paralleled by differences in blood-spinal cord barrier (BSCB) repair in the two mouse strains. We conducted spinal cord compression injuries in knock-out and wild-type mice. BSCB permeability was assessed by measuring the Evans blue spread within the spinal cord tissue at 14-21 days after injury. Results show that CHL1 reduces and tenascin-C enhances BSCB permeability, suggesting a correlation between functional outcome and BSCB repair.

• Authors: Nicole R Peter, Ronak T Shah, Jian Chen, Andrey Irintchev, Melitta Schachner
• Journal: Neuroreport (Neuroreport) Vol. 23 Issue 8 Pg. 479-82 (May 30 2012) ISSN: 1473-558X [Electronic] England
• PMID: 22473292 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Cell Adhesion Molecules
• Chl1 protein, mouse
• Tenascin
• Evans Blue

Topics

• Analysis of Variance
• Animals
• Cell Adhesion Molecules (deficiency, metabolism)
• Disease Models, Animal
• Evans Blue
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Microvessels (drug effects, pathology, physiopathology)
• Permeability
• Recovery of Function (genetics)
• Spinal Cord (metabolism)
• Spinal Cord Injuries (pathology, physiopathology)
• Spinal Cord Regeneration (genetics)
• Tenascin (deficiency, metabolism)
• Time Factors