title: Absence of galectin-3 promotes neuroprotection in retinal ganglion cells after optic nerve injury.
abstract: A trauma to the mature central nervous system (CNS) often leads to persistent deficits, due to the inability of axons to regenerate after being injured. Increasing evidence suggests that pro-inflammatory and pro-apoptotic genes can present a major obstacle to promoting neuroprotection of retinal ganglion cells and consequently succeed in axonal regeneration. This study evaluated the effect of the absence of galectin-3 (Gal-3) on retinal ganglion cells (RGC) survival and axonal regeneration/degeneration after optic nerve crush injury. Two weeks after crush there was a 2.6 fold increase in the rate of cell survival in Gal-3-/- mice (1283±79.15) compared to WT animals (495.4±53.96). However, no regeneration was observed in the Gal-3-/- mice two weeks after lesion. Furthermore, axonal degeneration presented a particular pattern on those mice; Electron Microscopy (EM) analysis showed incomplete axon degeneration while the WT mice presented an advanced stage of degeneration. This suggests that the removal of the nerve fibers in the Gal 3-/- mice could be deficient and this would cause a delay in the process of Wallerian degeneration once there is a decrease in the number of macrophages/microglia in the nerve. This study demonstrates how the absence of Gal-3 can affect RGC survival and optic nerve regeneration/degeneration after lesion. Our results suggest that the absence of Gal-3 plays an important role in the survival of RGC and thus can be a potential target for therapeutic intervention in RGC neuroprotection.
authors.affiliation: Department of Pathology, Medical College, HUCFF, UFRJ, Rio de Janeiro, Brazil.|Laboratory of Neurodegeneration and Repair, Medical College, HUCFF, UFRJ, Rio de Janeiro, Brazil.
authors.forename: Carla Andreia
authors.initials: CA
authors.lastname: Abreu
authors.affiliation: Laboratory of Neurodegeneration and Repair, Medical College, HUCFF, UFRJ, Rio de Janeiro, Brazil.
authors.forename: Silmara Veline
authors.initials: SV
authors.lastname: De Lima
authors.affiliation: Department of Pathology, Medical College, HUCFF, UFRJ, Rio de Janeiro, Brazil.|Laboratory of Neurodegeneration and Repair, Medical College, HUCFF, UFRJ, Rio de Janeiro, Brazil.
authors.forename: Henrique Rocha
authors.initials: HR
authors.lastname: Mendonça
authors.affiliation: Department of Pathology, Medical College, HUCFF, UFRJ, Rio de Janeiro, Brazil.|Laboratory of Neurodegeneration and Repair, Medical College, HUCFF, UFRJ, Rio de Janeiro, Brazil.
authors.forename: Camila de Oliveira
authors.initials: CO
authors.lastname: Goulart
authors.affiliation: Postgraduate in Anatomical Pathology, Department of Pathology, Medical College, HUCFF, UFRJ, Rio de Janeiro, Brazil.|Laboratory of Neurodegeneration and Repair, Medical College, HUCFF, UFRJ, Rio de Janeiro, Brazil. martinez@histo.ufrj.br.
authors.forename: Ana Maria Blanco
authors.initials: AM
authors.lastname: Martinez
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D037502:Galectin 3 / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D046529:Microscopy, Electron, Transmission; D009409:Nerve Crush; D009410:Nerve Degeneration / Q000378:metabolism; D009416:Nerve Regeneration / Q000502:physiology*; D000066829:Neuroprotection / Q000502:physiology*; D020221:Optic Nerve Injuries / Q000378:metabolism / Q000473:pathology*; D012165:Retinal Ganglion Cells / Q000378:metabolism / Q000473:pathology*
chemical_list: D037502:Galectin 3; C485095:Lgals3 protein, mouse