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 3–28 days post-injury (dpi), and in ˜ 45% of astrocytes in the lesion border at 7–28 dpi. 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.