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Galectin‐1 deficiency improves axonal swelling of motor neurones in SOD 1 G93A transgenic mice
Author(s) -
Kobayakawa Yuko,
Sakumi Kunihiko,
Kajitani Kosuke,
Kadoya Toshihiko,
Horie Hidenori,
Kira Junichi,
Nakabeppu Yusaku
Publication year - 2015
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/nan.12123
Subject(s) - gliosis , genetically modified mouse , sod1 , amyotrophic lateral sclerosis , neurofilament , biology , astrocyte , spinal cord , microbiology and biotechnology , motor neuron , pathology , neuroscience , transgene , central nervous system , immunology , medicine , biochemistry , immunohistochemistry , disease , gene
Aims Galectin‐1, a member of the β‐galactoside‐binding lectin family, accumulates in neurofilamentous lesions in the spinal cords of both sporadic and familial amyotrophic lateral sclerosis ( ALS ) patients with a superoxide dismutase 1 gene ( SOD1 ) mutation ( A 4 V ). The aim of this study was to evaluate the roles of endogenous galectin‐1 in the pathogenesis of ALS . Methods Expression of galectin‐1 in the spinal cord of mutant SOD 1 transgenic ( SOD 1 G93A ) mice was examined by pathological analysis, real‐time RT ‐ PCR and W estern blotting. The effects of galectin‐1 deficiency were evaluated by cross‐breeding SOD 1 G93A mice with galectin‐1 null ( Lgals1 −/− ) mice. Results Before ALS ‐like symptoms developed in SOD 1 G93A / Lgals1 +/+ mice, strong galectin‐1 immunoreactivity was observed in swollen motor axons and colocalized with aggregated neurofilaments. Electron microscopic observations revealed that the diameters of swollen motor axons in the spinal cord were significantly smaller in SOD 1 G93A / Lgals1 −/− mice, and there was less accumulation of vacuoles compared with SOD 1 G93A / Lgals1 +/+ mice. In symptomatic SOD 1 G93A / Lgals1 +/+ mice, astrocytes surrounding motor axons expressed a high level of galectin‐1. Conclusions Galectin‐1 accumulates in neurofilamentous lesions in SOD 1 G93A mice, as previously reported in humans with ALS . Galectin‐1 accumulation in motor axons occurs before the development of ALS ‐like symptoms and is associated with early processes of axonal degeneration in SOD 1 G93A mice. In contrast, galectin‐1 expressed in astrocytes may be involved in axonal degeneration during symptom presentation.