Absence of galectin-3 promotes neuroprotection in retinal ganglion cells after optic nerve injury
Carla Andreia Abreu1,2, Silmara Veline De Lima2, Henrique Rocha Mendonça1,2, Camila de Oliveira Goulart1,2 and Ana Maria Blanco Martinez1,2
1Postgraduate in Anatomical Pathology, Department of Pathology and 2Laboratory of Neurodegeneration and Repair, Medical College, HUCFF, UFRJ, Rio de Janeiro, RJ, Brazil
Offprint requests to: Ana Maria Blanco Martinez, Av. Professor Rodolpho Paulo Rocco, 255 CCS Bloco F2-012. Ilha do Fundão. 21941-902, Rio de Janeiro-RJ, Brazil. email: martinez@histo.ufrj.br
Summary. 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. Histol Histopathol 32, 253-262 (2017)
Key words: Retinal ganglion cells, Optic nerve, Galectin-3, Wallerian Degeneration
DOI: 10.14670/HH-11-788