Effects of Galectin-1 on the Inflammatory Response of Macrophages and Astrocytes following Spinal Cord Injury in Rats
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After traumatic spinal cord injury (SCI) tissue repair and functional recovery are minimal. This is partially due to the primary lesion, and is exacerbated by secondary injury resulting from the inflammatory response triggered by damage. Astrocytes and macrophages are inflammatory cell types present after SCI that have beneficial and detrimental effects on recovery. The protein galectin-1 has been shown to drive the beneficial response of these cells, stimulating astrocytes to secrete bone-derived neurotropic factor (BDNF) to promote neuronal survival and inducing macrophages to secrete axonal-regeneration promoting factors. In addition, oxidized galectin-1 shifts macrophages from the neurotoxic (M1) to neuroprotective (M2) phenotype. In this study, we hypothesized that addition of oxidized galectin-1 to the site of SCI will improve recovery. We induced spinal cord injury in rats, administered treatments through an osmotic mini-pump, and examined functional recovery. Immunohistochemistry and examination of mRNA levels of inflammatory markers were performed on untreated rat and mouse spinal cord tissue. In vivo galectin-1 treatments did not result in differences in functional recovery scores. Galectin-1 increased after injury in untreated animals and colocalized with macrophage and astrocyte markers. While our study found an increase in the expression of M1 macrophage markers, M2 macrophage markers, and galectin-1 markers in spinal cord tissue mRNA in early time points post-injury, we did not find increased presence of galectin-1 colocalizing with cultured M2 bone marrow derived macrophages which would be expected if a shift from M1 to M2 macrophage phenotype occurred. The potential role of galectin-1 in enhancing healing and functional recovery after SCI remains a possibility. Future studies should aim to uncover the role of this protein and whether it is an effective treatment for SCI.