title: Lack of galectin-3 improves the functional outcome and tissue sparing by modulating inflammatory response after a compressive spinal cord injury.
abstract: Spinal cord injury (SCI) is a traumatic event that results in motor, sensitive or autonomic function disturbances, which have direct impact on the life quality of the affected individual. Recent studies have shown that attenuation of the inflammatory response after SCI plays a key role in the reestablishment of motor function. Galectin-3 is a pleiotropic molecule belonging to the carbohydrate-ligand lectin family, which is expressed by different cells in different tissues. Studies have shown that galectin-3 induces the recruitment and activation of neutrophils, monocytes/macrophages, lymphocytes and microglia. Thus, the aim of this study was to evaluate the effects of the lack of galectin-3 on the functional outcome, cellular recruitment and morphological changes in tissue, after SCI. C57BL/6 wild-type and galectin-3 knockout mice were used in this study. A vascular clip was used for 1 min to generate a compressive SCI. By BMS we detected that the Gal-3(-/-) presented a better functional outcome during the studied period. This finding is related to a decrease in the injury length and a higher volume of spared white matter at 7 and 42 days post injury (dpi). Moreover, Gal-3(-/-) mice showed a higher number of spared fibers at 28 dpi. Because of the importance of the inflammatory response after SCI and the role that galectin-3 plays in it, we investigated possible differences in the inflammatory response between the analyzed groups. No differences in neutrophils were observed 24h after injury. However, at 3 dpi, the Gal-3(-/-) mice showed more neutrophils infiltrated into the spinal tissue when compared with the WT mice. At this same time point, no differences in the percentage of the CD11b/Arginase1 positive cells were observed. Remarkably, Gal-3(-/-) mice displayed a decrease in CD11b staining at 7 dpi, compared with the WT mice. At the same time, Gal-3(-/-) mice presented a more prominent Arginase1 stained area, suggesting an anti-inflammatory cell phenotype. Taken together, these results demonstrated that the lack of galectin-3 plays a key role in the inflammatory process triggered by SCI, leading to better and early recovery of locomotor function.
authors.affiliation: Laboratório de Neurodegeneração e Reparo, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Avenida Carlos Chagas Filho, 373, CCS, Cidade Universitária, Rio de Janeiro, RJ21941-902, Brazil; Laboratório de Neurodegeneração e Reparo, Faculdade de Medicina, Departamento de Patologia, HUCFF, Universidade Federal do Rio de Janeiro, Avenida Carlos Chagas Filho, 373, CCS, Cidade Universitária, Rio de Janeiro, RJ21941-902, Brazil. Electronic address: klaussmostacada@histo.ufrj.br.
authors.forename: Klauss
authors.initials: K
authors.lastname: Mostacada
authors.affiliation: Laboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Avenida Carlos Chagas Filho, 373, CCS, Cidade Universitária, Rio de Janeiro, RJ21941-902, Brazil. Electronic address: felipe@histo.ufrj.br.
authors.forename: Felipe L
authors.initials: FL
authors.lastname: Oliveira
authors.affiliation: Laboratório de Pesquisas sobre o Timo, Instituto Oswaldo Cruz, Fiocruz, Avenida Brasil, 4365, Pavilhão Leônidas Deane, sala 510, Manguinhos, Rio de Janeiro, RJ21040-360, Brazil. Electronic address: dvv@ioc.fiocruz.br.
authors.forename: Déa M S
authors.initials: DM
authors.lastname: Villa-Verde
authors.affiliation: Laboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Avenida Carlos Chagas Filho, 373, CCS, Cidade Universitária, Rio de Janeiro, RJ21941-902, Brazil. Electronic address: martinez@histo.ufrj.br.
authors.forename: Ana Maria Blanco
authors.initials: AM
authors.lastname: Martinez
mesh_terms: D000818:Animals; D001119:Arginase / Q000378:metabolism; D039481:CD11b Antigen / Q000378:metabolism; D004195:Disease Models, Animal; D005106:Exploratory Behavior / Q000502:physiology; D005260:Female; D037502:Galectin 3 / Q000172:deficiency* / Q000235:genetics; D005786:Gene Expression Regulation / Q000235:genetics; D007211:Indoles / Q000378:metabolism; D007249:Inflammation / Q000209:etiology*; D008214:Lymphocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D017628:Microglia / Q000473:pathology; D009043:Motor Activity / Q000502:physiology; D009504:Neutrophils / Q000473:pathology; D020127:Recovery of Function / Q000235:genetics*; D013117:Spinal Cord Compression / Q000150:complications* / Q000473:pathology*
chemical_list: D039481:CD11b Antigen; D037502:Galectin 3; D007211:Indoles; C018588:Luxol Fast Blue MBS; C544448:Arg1 protein, mouse; D001119:Arginase
keywords: Galectin-3; Macrophages; Mice; Microglia; Neuroinflammation; Neutrophils; Spinal cord injury (SCI)