Galectin-1 in injured rat spinal cord: Implications for macrophage phagocytosis and neural repair

Galectin (Gal)-1 is a small carbohydrate-binding protein and immune modulatory cytokine that is synthesized locally at the site of peripheral nerve injury. In this environment, Gal1 can promote regeneration of injured peripheral axons, in part by modifying the function of macrophages recruited to th...

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Bibliographic Details
Published in:Molecular and cellular neuroscience 2015-01, Vol.64, p.84-94
Main Authors: Gaudet, Andrew D., Sweet, David R., Polinski, Nicole K., Guan, Zhen, Popovich, Phillip G.
Format: Article
Language:English
Subjects:
Animals
Astrocytes - metabolism
Extracellular matrix
Female
Galectin 1 - genetics
Galectin 1 - metabolism
Glial scar
Inflammation
Macrophages - metabolism
Neuroinflammation
Phagocytosis
Rats
Rats, Sprague-Dawley
Spinal Cord Injuries - metabolism
Spinal cord injury
Spinal Cord Regeneration
Up-Regulation
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Summary:Galectin (Gal)-1 is a small carbohydrate-binding protein and immune modulatory cytokine that is synthesized locally at the site of peripheral nerve injury. In this environment, Gal1 can promote regeneration of injured peripheral axons, in part by modifying the function of macrophages recruited to the site of injury. Unlike in injured peripheral nerves, macrophages do not promote axon regeneration in the injured central nervous system (CNS), perhaps because Gal1 levels are not regulated appropriately. Because the dynamics and cellular localization of endogenous Gal1 have not been rigorously characterized after CNS injury, we examined the spatio-temporal distribution of Gal1 in rat spinal cords subjected to a standardized contusion injury. Whereas Gal1 was not expressed in uninjured spinal cord, it was significantly upregulated after SCI, especially within the lesion core. Gal1 was expressed in ~40% of lesion-localized macrophages at 3–28days post-injury (dpi), and in ~45% of astrocytes in the lesion border at 7–28dpi. Most lesion-localized Gal1+ macrophages did not express the phagocytosis marker ED1, and Gal1+ cells contained less phagocytosed lipids. These data suggest that time- and location-dependent regulation of Gal1 by macrophages (and astrocytes) could be important for modulating phagocytosis, inflammation/gliosis, and axon growth after SCI. •After spinal cord injury, galectin-1 is strongly upregulated.•45% of astrocytes within the glial scar are galectin-1+ by 7days post-injury.•40% of macrophages in the injury epicenter are galectin-1+ by 3days post-injury.•Galectin-1 is negatively correlated with macrophage phagocytic potential.•Injury-induced galectin-1 may regulate debris removal and matrix remodeling.
ISSN:1044-7431
1095-9327
DOI:10.1016/j.mcn.2014.12.006